Статті в журналах: "Streptococcus pneumoniae – immunologie"

1

Palmer, D. L. "Laboratory Diagnosis of Streptococcus pneumoniae Pneumonia." Journal of Infectious Diseases 151, no. 2 (February 1, 1985): 378. http://dx.doi.org/10.1093/infdis/151.2.378.

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Abateneh, Dejene Derseh, Abera Kumalo Shano, and Teshale Worku Dedo. "Nasopharyngeal Carriage of Streptococcus pneumoniae and Associated Factors among Children in Southwest Ethiopia." Open Microbiology Journal 14, no. 1 (July 30, 2020): 171–78. http://dx.doi.org/10.2174/1874285802014010171.

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Background: In Ethiopia, Streptococcus pneumoniae is the predominant causative agent of pneumonia. About, 95% of bacterial pneumonia cases in under five years of children are caused by pneumococci. Objective: To assess the nasopharyngeal carriage of Streptococcus pneumoniae, its antibiotic susceptibility pattern, and associated factors among children in Southwest Ethiopia. Methods: A cross-sectional study was conducted from October 01, 2018, to December 30, 2018. A total of 293 children aged ≤15 years were included in the study using a systematic random sampling technique. A nasopharyngeal swab was collected using a sterile cotton swab and cultured on blood agar supplemented with 5μg/ml gentamicin. The antimicrobial susceptibility testing was performed using the Kirby-Bauer disc diffusion technique. Results: The ages of participants ranged from 5 months to 14 years. The carriage rate of Streptococcus pneumoniae was 74/293 (25.3%). Being within the age group <3 years, the habit of sleeping with parent(s)/guardians and numbers of rooms per household were significantly associated with pneumococcal carriage. Streptococcus pneumoniae showed the highest resistance to Tetracycline, 36 (48.65%), and Trimethoprim/sulfamethoxazole, 29 (39.2%), and was found to be susceptible to Chloramphenicol, 54 (77%), and Erythromycin, 38 (51.4%). Conclusion: The nasopharyngeal carriage rate of Streptococcus pneumoniae is considerably high. High antimicrobial resistance of Streptococcus pneumoniae against Tetracycline and Trimethoprim/sulfamethoxazole was observed. Living in a house with a single room, children’s habit of sleeping with parents/guardians and age are associated factors of high pneumococcal carriage. Strategies need to be designed to address the modifiable associated factors and the bacterium antibiotic resistance pattern should be monitored regularly.

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Ahn, Danielle, and Alice Prince. "Participation of Necroptosis in the Host Response to Acute Bacterial Pneumonia." Journal of Innate Immunity 9, no. 3 (2017): 262–70. http://dx.doi.org/10.1159/000455100.

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Common pulmonary pathogens, such as Streptococcus pneumoniae and Staphylococcus aureus, as well as the host-adapted pathogens responsible for health care-associated pneumonias, such as the carbapenem-resistant Klebsiella pneumoniae and Serratia marcecsens, are able to activate cell death through the RIPK1/RIPK3/MLKL cascade that causes necroptosis. Necroptosis can influence the pathogenesis of pneumonia through several mechanisms. Activation of this pathway can result in the loss of specific types of immune cells, especially macrophages, and, in so doing, contribute to host pathology through the loss of their critical immunoregulatory functions. However, in other settings of infection, necroptosis promotes pathogen removal and the eradication of infected cells to control excessive proinflammatory signaling. Bacterial production of pore-forming toxins provides a common mechanism to activate necroptosis by diverse bacterial species, with variable consequences depending upon the specific pathogen. Included in this brief review are data demonstrating the ability of the carbapenem-resistant ST258 K. pneumoniae to activate necroptosis in the setting of pneumonia, which is counterbalanced by their suppression of CYLD expression. Exactly how necroptosis and other mechanisms of cell death are coregulated in the response to specific pulmonary pathogens remains a topic of active investigation, and it may provide potential therapeutic targets in the future.

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Briones, Maria Luisa, José Blanquer, David Ferrando, Maria Luisa Blasco, Concepción Gimeno, and Julio Marín. "Assessment of Analysis of Urinary Pneumococcal Antigen by Immunochromatography for Etiologic Diagnosis of Community-Acquired Pneumonia in Adults." Clinical and Vaccine Immunology 13, no. 10 (October 2006): 1092–97. http://dx.doi.org/10.1128/cvi.00090-06.

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ABSTRACT The limitations of conventional microbiologic methods (CMM) for etiologic diagnosis of community pneumococcal pneumonia have made faster diagnostic techniques necessary. Our aim was to evaluate the usefulness of the immunochromatography (ICT) technique for detecting urinary Streptococcus pneumoniae antigen in the etiologic diagnosis of community-acquired pneumonias (CAP). This was a prospective study on in-patients with CAP in a tertiary hospital conducted from October 2000 to March 2004. Apart from using CMM to reach an etiologic diagnosis, we determined pneumococcal antigen in concentrated urine by ICT. We also determined the urinary pneumococcal antigen (UPA) content in patients from two control groups to calculate the specificity of the technique. One group was comprised of in-patients diagnosed with chronic obstructive pulmonary disease (COPD) or asthma, with respiratory infection, and without pneumonia; the other group included fractures. We studied 959 pneumonia patients and determined UPA content in 911 (95%) of them. We diagnosed the etiology of 253 cases (28%) using CMM; S. pneumoniae was the most common etiologic agent (57 cases). ICT analysis was positive for 279 patients (31%). Using this technique, the percentage of diagnoses of pneumococcal pneumonias increased by 26%, while the overall etiologic diagnosis increased from 28 to 49%. The technique sensitivity was 81%; the specificity oscillated between 80% in CAP with nonpneumococcal etiology and 99% for patients with fractures without infections. Determination of UPA is a rapid, simple analysis with good sensitivity and specificity, which increased the percentage of etiologic diagnoses. Positive UPA may persist in COPD patients with probable pneumococcal colonization or recent pneumococcal infections.

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Mizgerd, J. P., B. B. Meek, G. J. Kutkoski, D. C. Bullard, A. L. Beaudet, and C. M. Doerschuk. "Selectins and neutrophil traffic: margination and Streptococcus pneumoniae-induced emigration in murine lungs." Journal of Experimental Medicine 184, no. 2 (August 1, 1996): 639–45. http://dx.doi.org/10.1084/jem.184.2.639.

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The roles of selectins in the pulmonary margination and emigration of neutrophils were investigated by using mice genetically deficient in both E- and P-selectins (E/P mutants) and/or by intravenous injections of fucoidin (inhibiting both L- and P-selectins). E/P mutants were neutrophilic (14.7 +/- 4.9 x 10(6) vs. 0.8 +/- 0.1 x 10(6) neutrophils/ml). This neutrophilia was associated with increased margination of neutrophils within pulmonary capillaries (39.7 +/- 9.4 vs. 4.6 +/- 1.1 neutrophil profiles per 100 red blood cell profiles) but no change in margination within noncapillary pulmonary microvessels. After intratracheal instillation of Streptococcus pneumoniae, lungs of E/P mutants displayed increased neutrophil emigration (564 +/- 92 vs. 116 +/- 19 neutrophils per 100 alveolar profiles), edema (5.3 +/- 1.5 vs. 1.5 +/- 0.4 microliter/g body weight), and histologic evidence of lung injury compared with those in wild-type (WT). Fucoidin treatment did not affect neutrophil emigration during streptococcal pneumonia in WT or E/P mice. During pneumonia, the number of white blood cells (WBC) tethered to or spread upon the noncapillary vessel endothelium increased in both WT and E/P lungs. These are the first data demonstrating that neutrophil margination in uninfected pulmonary capillaries does not require E- and P-selectins; that streptococcal pneumonia induces an E- and P-selectin-independent increase in WBC interactions with noncapillary endothelium; and that migration of neutrophils to alveoli can occur despite deficiency or inhibition of all of the known selectins.

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Peng, Xin, Yi Wu, Xiao Kong, Yunxiu Chen, Yonglu Tian, Qinyuan Li, Xiaoyin Tian, Guangli Zhang, Luo Ren, and Zhengxiu Luo. "Neonatal Streptococcus pneumoniae Pneumonia Induces an Aberrant Airway Smooth Muscle Phenotype and AHR in Mice Model." BioMed Research International 2019 (January 6, 2019): 1–8. http://dx.doi.org/10.1155/2019/1948519.

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Our previous study showed that neonatal S. pneumoniae infection aggravated airway inflammation and airway hyperresponsiveness (AHR) in an OVA-induced allergic asthma model. As airway smooth muscle (ASM) plays a pivotal role in AHR development, we aim to investigate the effects of neonatal S. pneumoniae pneumonia on ASM structure and AHR development. Non-lethal neonatal pneumonia was established by intranasally infecting 1-week-old BALB/C mice with the S. pneumoniae strain D39. Five weeks after infection, the lungs were collected to assess the levels of α-SMA and the contractile proteins of ASM. Our results indicate that neonatal S. pneumoniae pneumonia significantly increased adulthood lung α-SMA and SMMHC proteins production and aggravated airway inflammatory cells infiltration and cytokines release. In addition, the neonatal S. pneumoniae pneumonia group had significantly higher Penh values compared to the uninfected controls. These data suggest that neonatal S. pneumoniae pneumonia promoted an aberrant ASM phenotype and AHR development in mice model.

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Tanaka, Akitaka, Shigeki Nakamura, Masafumi Seki, Kenji Fukudome, Naoki Iwanaga, Yoshifumi Imamura, Taiga Miyazaki, et al. "Toll-Like Receptor 4 Agonistic Antibody Promotes Innate Immunity against Severe Pneumonia Induced by Coinfection with Influenza Virus and Streptococcus pneumoniae." Clinical and Vaccine Immunology 20, no. 7 (May 1, 2013): 977–85. http://dx.doi.org/10.1128/cvi.00010-13.

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ABSTRACTCoinfection with bacteria is a major cause of mortality during influenza epidemics. Recently, Toll-like receptor (TLR) agonists were shown to have immunomodulatory functions. In the present study, we investigated the effectiveness and mechanisms of the new TLR4 agonistic monoclonal antibody UT12 against secondary pneumococcal pneumonia induced by coinfection with influenza virus in a mouse model. Mice were intranasally inoculated withStreptococcus pneumoniae2 days after influenza virus inoculation. UT12 was intraperitoneally administered 2 h before each inoculation. Survival rates were significantly increased and body weight loss was significantly decreased by UT12 administration. Additionally, the production of inflammatory mediators was significantly suppressed by the administration of UT12. In a histopathological study, pneumonia in UT12-treated mice was very mild compared to that in control mice. UT12 increased antimicrobial defense through the acceleration of macrophage recruitment into the lower respiratory tract induced by c-Jun N-terminal kinase (JNK) and nuclear factor kappaB (NF-κB) pathway-dependent monocyte chemoattractant protein 1 (MCP-1) production. Collectively, these findings indicate that UT12 promoted pulmonary innate immunity and may reduce the severity of severe pneumonia induced by coinfection with influenza virus andS. pneumoniae. This immunomodulatory effect of UT12 improves the prognosis of secondary pneumococcal pneumonia and makes UT12 an attractive candidate for treating severe infectious diseases.

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8

Muñoz, Natalia, Laurye Van Maele, Juan M. Marqués, Analía Rial, Jean-Claude Sirard, and José A. Chabalgoity. "Mucosal Administration of Flagellin Protects Mice from Streptococcus pneumoniae Lung Infection." Infection and Immunity 78, no. 10 (July 19, 2010): 4226–33. http://dx.doi.org/10.1128/iai.00224-10.

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ABSTRACT Streptococcus pneumoniae is a major cause of pneumonia in infants and the elderly. Innate defenses are essential to the control of pneumococcal infections, and deficient responses can trigger disease in susceptible individuals. Here we showed that flagellin can locally activate innate immunity and thereby increase the resistance to acute pneumonia. Flagellin mucosal treatment improved S. pneumoniae clearance in the lungs and promoted increased survival of infection. In addition, lung architecture was fully restored after the treatment of infected mice, indicating that flagellin allows the reestablishment of steady-state conditions. Using a flagellin mutant that is unable to signal through Toll-like receptor 5 (TLR5), we established that TLR5 signaling is essential for protection. In the respiratory tract, flagellin induced neutrophil infiltration into airways and upregulated the expression of genes coding for interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), CXCL1, CXCL2, and CCL20. Using depleting antibodies, we demonstrated that neutrophils are major effectors of protection. Further, we found that B- and T-cell-deficient SCID mice clear S. pneumoniae challenge to the same extent as immunocompetent animals, suggesting that these cell populations are not required for flagellin-induced protection. In conclusion, this study emphasizes that mucosal stimulation of innate immunity by a TLR not naturally engaged by S. pneumoniae can increase the potential to cure pneumococcal pneumonia.

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9

Jahan, Rownak, Shirin Tarafder, and Anwarul Haque. "Aetiological ahents of Adult Bacterial Pneumonia parients admitted at a Tertiary Care Hospital in Dhaka city." Journal of Shaheed Suhrawardy Medical College 7, no. 1 (March 7, 2017): 22–25. http://dx.doi.org/10.3329/jssmc.v7i1.31786.

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Background: Bacterial pneumonia is one of the most common causes of mortality and morbidity worldwide especially in adults.Objective: The purpose of this present study was to identify the aetiological agents and antimicrobial sensitivity pattern of bacterial pneumonia in patients admitted at intensive care unit (ICU).Methodology: This cross sectional study was carried out in the Department of Microbiology & Immunology at Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka, Bangladesh from August 2012 to July 2013. Blood and tracheal aspirates (TA) culture were done in clinically diagnosed pneumonia patients admitted in the ICU of BSMMU. PCR of TA was performed to identify Legionella species. Urine ICT of patients was done to detect Streptococcus pneumoniae and Legionella pneumophila serogroup 1 antigens. Antimicrobial susceptibility of isolated bacteria was done by disc diffusion method.Result: A total of 36 pneumonia patients admitted at ICU were recruited. The most common identified bacteria were Acinetobacter species (33.3%) followed by Pseudomonas species (30.5%), Klebsiella pneumoniae (11.1%), Escherichia coli (5.5%), Enterobacter aerogenes (5.5%), Legionella (8.3%), Citrobacterfreundii (2.8%) and Proteus mirabilis (2.8%). Majority of the bacteria were resistant to first line antibiotics and highly sensitive to carbapenems.Conclusion: Most common isolated bacteria are the Acinetobacter species, Pseudomonas species and Klebsiella pneumoniae among the pneumonic patients with the resistant to first line antibiotics and sensitive to carbapenems.J Shaheed Suhrawardy Med Coll, 2015; 7(1):22-25

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10

Gubba, Siddeswar, Donald E. Low, and James M. Musser. "Expression and Characterization of Group AStreptococcus Extracellular Cysteine Protease Recombinant Mutant Proteins and Documentation of Seroconversion during Human Invasive Disease Episodes." Infection and Immunity 66, no. 2 (February 1, 1998): 765–70. http://dx.doi.org/10.1128/iai.66.2.765-770.1998.

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ABSTRACT A recent study with isogenic strains constructed by recombinant DNA strategies unambiguously documented that a highly conserved extracellular cysteine protease expressed by Streptococcus pyogenes (group A Streptococcus [GAS]) is a critical virulence factor in a mouse model of invasive disease (S. Lukomski, S. Sreevatsan, C. Amberg, W. Reichardt, M. Woischnik, A. Podbielski, and J. M. Musser, J. Clin. Invest. 99:2574–2580, 1997). To facilitate further investigations of the streptococcal cysteine protease, recombinant proteins composed of a 40-kDa zymogen containing a C192S amino acid substitution that ablates enzymatic activity, a 28-kDa mature protein with the C192S replacement, and a 12-kDa propeptide were purified from Escherichia colicontaining His tag expression vectors. The recombinant C192S zymogen retained apparently normal structural integrity, as assessed by the ability of purified wild-type streptococcal cysteine protease to process the 40-kDa molecule to the 28-kDa mature form. All three recombinant purified proteins retained immunologic reactivity with polyclonal and monoclonal antibodies. Humans with a diverse range of invasive disease episodes (erysipelas, cellulitis, pneumonia, bacteremia, septic arthritis, streptococcal toxic shock syndrome, and necrotizing fasciitis) caused by six distinct M types of GAS seroconverted to the streptococcal cysteine protease. These results demonstrate that this GAS protein is expressed in vivo during the course of human infections and thereby provide additional evidence that the cysteine protease participates in host-pathogen interactions in some patients.

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11

Hofstra, J. J., F. E. van den Boogaard, A. D. Cornet, A. P. J. Vlaar, T. van der Poll, M. Levi, and M. J. Schultz. "Inhibition of Pulmonary Coagulopathy by Nebulized Natural Anticoagulants during Streptococcus Pneumoniae Pneumonia in Rats." Blood 112, no. 11 (November 16, 2008): 3068. http://dx.doi.org/10.1182/blood.v112.11.3068.3068.

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Abstract RATIONALE: Alveolar fibrin deposition is intrinsic to pneumonia and acute lung injury. Activation of coagulation during pulmonary inflammation is primarily mediated by the tissue factor–factor VIIa pathway. Tissue factor levels in the lungs increase during pulmonary inflammation due to disruption of endothelial–epithelial barrier and expression of tissue factor on alveolar macrophages. Intravenous infusion of the natural anticoagulants activated protein C (APC) or antithrombin (AT) has been shown to have lung–protective effects in critically ill patients, but increases the risk of severe bleeding. Local administration may allow for higher treatment dosages and increased local efficacy while at the same time reducing the risk of bleeding. We evaluated the effect of nebulized tissue factor pathway inhibitor (TFPI), APC or AT on pulmonary coagulopathy and inflammation in a rat model of Streptococcus pneumoniae pneumonia. DESIGN: Randomized controlled in vivo study in a rat model of S. pneumoniae pneumonia. Twenty–eight male Sprague–Dawley rats were challenged intratracheally with S. pneumoniae (serotype 3, 106 colony forming units), inducing pneumonia. Rats were randomized to nebulization with TFPI, APC, AT or normal saline. RESULTS: Rats infected with S. pneumoniae had increased pulmonary and systemic levels of thrombin–antithrombin complexes (TATc) and fibrin degradation products (FDP), indicating increased coagulation. Simultaneously, pulmonary plasminogen activator inhibitor 1 (PAI–1) activity was increased and plasminogen activator activity (PAA) was reduced, indicating inhibition of endogenous fibrinolysis. Treatment with any nebulized natural anticoagulant significantly attenuated the rise in bronchoalveolar TATc (3.5 ± 0.9 ng/mL (TFPI), 3.6 ± 0.6 ng/mL (APC) and 4.6 ± 0.6 ng/mL (AT) versus 9.1 ± 0.75 ng/mL in saline treated rats, P<.01) and FDP (290 ± 92 ng/mL (TFPI), 310 ± 90 ng/mL (APC) and 158 ± 44 ng/mL (AT) versus 559 ± 116 ng/mL in saline treated rats, P<.01). TFPI and APC also significantly reduced systemic TATc levels while AT did not have any effect on systemic coagulopathy (17 ng/mL ± 3.4 (TFPI) and 13.8 ± 2.3 ng/mL (APC) versus 19.7 ± 1.6 ng/mL in saline treated rats, P<.05 and P<.01 respectively). While TFPI and APC did not affect host defense to S. pneumoniae, treatment with AT resulted in a reduction of bacterial outgrowth from the lungs, a reduction of neutrophil influx into the pulmonary compartment and less histopathologic lung injury. CONCLUSIONS: Nebulization of natural anticoagulants attenuates pulmonary coagulopathy during S. pneumoniae pneumonia. While APC and TFPI leaves local inflammation and host defense unaltered, AT exerts significant lung–protective effects in pneumococcal pneumonia in rats.

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van den Boogaard, Florry E., Xanthe Brands, Joris J. T. H. Roelofs, Regina de Beer, Onno J. de Boer, Cornelis van 't Veer, and Tom van der Poll. "Mast Cells Impair Host Defense During Murine Streptococcus pneumoniae Pneumonia." Journal of Infectious Diseases 210, no. 9 (May 13, 2014): 1376–84. http://dx.doi.org/10.1093/infdis/jiu285.

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13

Steinwede, Kathrin, Stefanie Henken, Jennifer Bohling, Regina Maus, Bianca Ueberberg, Christina Brumshagen, Erik L. Brincks, Thomas S. Griffith, Tobias Welte, and Ulrich A. Maus. "TNF-related apoptosis-inducing ligand (TRAIL) exerts therapeutic efficacy for the treatment of pneumococcal pneumonia in mice." Journal of Experimental Medicine 209, no. 11 (October 15, 2012): 1937–52. http://dx.doi.org/10.1084/jem.20120983.

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Apoptotic death of alveolar macrophages observed during lung infection with Streptococcus pneumoniae is thought to limit overwhelming lung inflammation in response to bacterial challenge. However, the underlying apoptotic death mechanism has not been defined. Here, we examined the role of the TNF superfamily member TNF-related apoptosis-inducing ligand (TRAIL) in S. pneumoniae–induced macrophage apoptosis, and investigated the potential benefit of TRAIL-based therapy during pneumococcal pneumonia in mice. Compared with WT mice, Trail−/− mice demonstrated significantly decreased lung bacterial clearance and survival in response to S. pneumoniae, which was accompanied by significantly reduced apoptosis and caspase 3 cleavage but rather increased necrosis in alveolar macrophages. In WT mice, neutrophils were identified as a major source of intraalveolar released TRAIL, and their depletion led to a shift from apoptosis toward necrosis as the dominant mechanism of alveolar macrophage cell death in pneumococcal pneumonia. Therapeutic application of TRAIL or agonistic anti-DR5 mAb (MD5-1) dramatically improved survival of S. pneumoniae–infected WT mice. Most importantly, neutropenic mice lacking neutrophil-derived TRAIL were protected from lethal pneumonia by MD5-1 therapy. We have identified a previously unrecognized mechanism by which neutrophil-derived TRAIL induces apoptosis of DR5-expressing macrophages, thus promoting early bacterial killing in pneumococcal pneumonia. TRAIL-based therapy in neutropenic hosts may represent a novel antibacterial treatment option.

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Kerr, Alison R., June J. Irvine, Jennifer J. Search, Neill A. Gingles, Aras Kadioglu, Peter W. Andrew, William L. McPheat, Charles G. Booth, and Tim J. Mitchell. "Role of Inflammatory Mediators in Resistance and Susceptibility to Pneumococcal Infection." Infection and Immunity 70, no. 3 (March 2002): 1547–57. http://dx.doi.org/10.1128/iai.70.3.1547-1557.2002.

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ABSTRACT Variations in the host response during pneumonia caused by Streptococcus pneumoniae in susceptible (CBA/Ca) and resistant (BALB/c) inbred mouse strains were investigated. Significant differences were detected in survival time, core body temperature, lung-associated and systemic bacterial loads, mast cell numbers, magnitude and location of cytokine production, lung disruption, and ability of isolated lung cells to release the cytokine tumor necrosis factor (TNF) alpha in vitro. Overall, the results indicate that the reduced capacity of CBA/Ca mice to induce rapid TNF activity within the airways following infection with S. pneumoniae may be a factor in their elevated susceptibility to pneumococcal pneumonia.

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Wang, Erjian, Nathalie Ouellet, Marie Simard, Isabelle Fillion, Yves Bergeron, Denis Beauchamp, and Michel G. Bergeron. "Pulmonary and Systemic Host Response to Streptococcus pneumoniae and Klebsiella pneumoniae Bacteremia in Normal and Immunosuppressed Mice." Infection and Immunity 69, no. 9 (September 1, 2001): 5294–304. http://dx.doi.org/10.1128/iai.69.9.5294-5304.2001.

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ABSTRACT Mortality related to bacteremic pneumonia remains high, and the role of sepsis in inflammation, pulmonary injury, and death remains unclear, mostly in leukopenic states. In the present study, the microbiology, histopathology, and host response to Streptococcus pneumoniae and Klebsiella pneumoniae infection were determined in an experimental model of bacteremia in immunocompetent and leukopenic mice. Leukocyte depletion by cyclophosphamide did not impair the early clearance of pneumococci from blood but facilitated growth in lungs. By contrast, klebsiellae rapidly grew in blood of leukopenic mice. These observations suggest that tissue-based phagocytes and circulating leukocytes, respectively, play prominent roles in S. pneumoniae and K. pneumoniaeeradication. The kinetics of leukocyte recruitment in lungs duringS. pneumoniae bacteremia suggested early strong inflammation in immunocompetent mice that is associated with tumor necrosis factor alpha release and histological disorders, including cell debris and surfactant in alveolar spaces. Leukocyte depletion further stimulated pulmonary capillary leakage both in S. pneumoniae and K. pneumoniae bacteremia, which seemed attributable to bacterial virulence factors. Nitric oxide production did not differ significantly among groups. Leukopenia and low platelet counts characterized the late stage of bacteremia for both strains, but only K. pneumoniae altered renal function. Understanding the pathogenesis of bacteremia will help establish beneficial therapies for both sepsis and pneumonia.

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Li, Yuanyuan, Ziyao Guo, Guangli Zhang, Xiaoyin Tian, Qinyuan Li, and Zhengxiu Luo. "Neonatal Streptococcus Pneumoniae pneumonia induces airway SMMHC expression through HMGB1/TLR4/ERK." Immunology Letters 240 (December 2021): 149–58. http://dx.doi.org/10.1016/j.imlet.2021.10.005.

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Batten, Margaret R., Bernard W. Senior, Mogens Kilian, and Jenny M. Woof. "Amino Acid Sequence Requirements in the Hinge of Human Immunoglobulin A1 (IgA1) for Cleavage by Streptococcal IgA1 Proteases." Infection and Immunity 71, no. 3 (March 2003): 1462–69. http://dx.doi.org/10.1128/iai.71.3.1462-1469.2003.

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ABSTRACT The amino acid sequence requirements in the hinge of human immunoglobulin A1 (IgA1) for cleavage by IgA1 proteases of different species of Streptococcus were investigated. Recombinant IgA1 antibodies were generated with point mutations at proline 227 and threonine 228, the residues lying on either side of the peptide bond at which all streptococcal IgA1 proteases cleave wild-type human IgA1. The amino acid substitutions produced no major effect upon the structure of the mutant IgA1 antibodies or their functional ability to bind to Fcα receptors. However, the substitutions had a substantial effect upon sensitivity to cleavage with some streptococcal IgA1 proteases, with, in some cases, a single point mutation rendering the antibody resistant to a particular IgA1 protease. This effect was least marked with the IgA1 protease from Streptococcus pneumoniae, which showed no absolute requirement for either proline or threonine at residues 227 to 228. By contrast, the IgA1 proteases of Streptococcus oralis, Streptococcus sanguis, and Streptococcus mitis had an absolute requirement for proline at 227 but not for threonine at 228, which could be replaced by valine. There was evidence in S. mitis that proteases from different strains may have different amino acid requirements for cleavage. Remarkably, some streptococcal proteases appeared able to cleave the hinge at a distant alternative site if substitution prevented efficient cleavage of the original site. Hence, this study has identified key residues required for the recognition of the IgA1 hinge as a substrate by streptococcal IgA1 proteases, and it marks a preliminary step towards development of specific enzyme inhibitors.

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Puzyreva, L. V., A. V. Mordyk, L. A. Rodkina, I. V. Zhitina, and A. V. Timofeeva. "Monitoring of opportunistic microflora in secondary respiratory infections of HIV-infected patients." HIV Infection and Immunosuppressive Disorders 12, no. 4 (February 9, 2021): 60–66. http://dx.doi.org/10.22328/2077-9828-2020-12-4-60-66.

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Objective: to evaluate the results of microbiological examination of sputum of HIV-infected patients with pneumonia clinic.Materials and methods. The analysis of microbiological results of sputum in 850 patients who were treated with pneumonia at the Infectious Clinical Hospital № 1 from 01.01.2012 to 01.01.2019.Results and its discussion. Gram-positive cocci were recorded in sputum in patients with HIV infection in 76,7±2,2% of cases. The growth of Staph. aureus noted in 20,1±2,0% of cases and was associated with the presence of sepsis and septic pneumonia. Staphylococcus epidermidis detected in sputum in 0,5±0,4% of HIV-positive patients with angiogenic sepsis. Streptococcus pyogenes was isolated in sputum in 2,3±0,8% of patients with severe community-acquired pneumonia. Str. pneumoniae was detected in 2,6±0,8% of cases. A common ﬁnding in the study of sputum in patients with HIV infection were viridans group Streptococci (50,3±2,6%). Gram-negative aerobic non-spore-forming bacterium Pseudomonas aeruginosa was found in 5,2±1,1%, Enterococcus faecalis in 3,1±0,9% of conﬁrmed cases of pneumonia. Klebsiella pneumonia was conﬁrmed in 11,5±1,6% of patients. Microbial association was noted in 24,1±1,7% of isolates; associations in combination with Staph. aureus were more common in 54,5±4,1% of HIV-infected patients with the clinic of community-acquired pneumonia.Conclusion. In patients with HIV infection with lung damage, it is necessary to collect biological material for microbiological examination, which will affect the further tactics of patient management.

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Phipps, John C., David M. Aronoff, Jeffrey L. Curtis, Deepti Goel, Edmund O'Brien, and Peter Mancuso. "Cigarette Smoke Exposure Impairs Pulmonary Bacterial Clearance and Alveolar Macrophage Complement-Mediated Phagocytosis of Streptococcus pneumoniae." Infection and Immunity 78, no. 3 (December 14, 2009): 1214–20. http://dx.doi.org/10.1128/iai.00963-09.

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ABSTRACT Cigarette smoke exposure increases the risk of pulmonary and invasive infections caused by Streptococcus pneumoniae, the most commonly isolated organism from patients with community-acquired pneumonia. Despite this association, the mechanisms by which cigarette smoke exposure diminishes host defense against S. pneumoniae infections are poorly understood. In this study, we compared the responses of BALB/c mice following an intratracheal challenge with S. pneumoniae after 5 weeks of exposure to room air or cigarette smoke in a whole-body exposure chamber in vivo and the effects of cigarette smoke on alveolar macrophage phagocytosis of S. pneumoniae in vitro. Bacterial burdens in cigarette smoke-exposed mice were increased at 24 and 48 h postinfection, and this was accompanied by a more pronounced clinical appearance of illness, hypothermia, and increased lung homogenate cytokines interleukin-1β (IL-1β), IL-6, IL-10, and tumor necrosis factor alpha (TNF-α). We also found greater numbers of neutrophils in bronchoalveolar lavage fluid recovered from cigarette smoke-exposed mice following a challenge with heat-killed S. pneumoniae. Interestingly, overnight culture of alveolar macrophages with 1% cigarette smoke extract, a level that did not affect alveolar macrophage viability, reduced complement-mediated phagocytosis of S. pneumoniae, while the ingestion of unopsonized bacteria or IgG-coated microspheres was not affected. This murine model provides robust additional support to the hypothesis that cigarette smoke exposure increases the risk of pneumococcal pneumonia and defines a novel cellular mechanism to help explain this immunosuppressive effect.

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Branger, Judith, Sylvia Knapp, Sebastiaan Weijer, Jaklien C. Leemans, Jennie M. Pater, Peter Speelman, Sandrine Florquin, and Tom van der Poll. "Role ofToll-Like Receptor 4 in Gram-Positive and Gram-Negative Pneumonia inMice." Infection and Immunity 72, no. 2 (February 2004): 788–94. http://dx.doi.org/10.1128/iai.72.2.788-794.2004.

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ABSTRACT To determine the role of Toll-like receptor 4 (TLR4) in the immune response to pneumonia, C3H/HeJ mice (which display a mutant nonfunctional TLR4) and C3H/HeN wild-type mice were intranasally infected with either Streptococcus pneumoniae (a common gram-positive respiratory pathogen) or Klebsiella pneumoniae (a common gram-negative respiratory pathogen). In cases of pneumococcal pneumonia, TLR4 mutant mice showed a reduced survival only after infection with low-level bacterial doses, which was associated with a higher bacterial burden in their lungs 48 h postinfection. In Klebsiella pneumonia, TLR4 mutant mice demonstrated a shortened survival after infection with either a low- or a high-level bacterial dose together with an enhanced bacterial outgrowth in their lungs. These data suggest that TLR4 contributes to a protective immune response in both pneumococcal and Klebsiella pneumonia and that its role is more important in respiratory tract infection caused by the latter (gram-negative) pathogen.

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Chiavolini, Damiana, Gianni Pozzi, and Susanna Ricci. "Animal Models of Streptococcus pneumoniae Disease." Clinical Microbiology Reviews 21, no. 4 (October 2008): 666–85. http://dx.doi.org/10.1128/cmr.00012-08.

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SUMMARY Streptococcus pneumoniae is a colonizer of human nasopharynx, but it is also an important pathogen responsible for high morbidity, high mortality, numerous disabilities, and high health costs throughout the world. Major diseases caused by S. pneumoniae are otitis media, pneumonia, sepsis, and meningitis. Despite the availability of antibiotics and vaccines, pneumococcal infections still have high mortality rates, especially in risk groups. For this reason, there is an exceptionally extensive research effort worldwide to better understand the diseases caused by the pneumococcus, with the aim of developing improved therapeutics and vaccines. Animal experimentation is an essential tool to study the pathogenesis of infectious diseases and test novel drugs and vaccines. This article reviews both historical and innovative laboratory pneumococcal animal models that have vastly added to knowledge of (i) mechanisms of infection, pathogenesis, and immunity; (ii) efficacies of antimicrobials; and (iii) screening of vaccine candidates. A comprehensive description of the techniques applied to induce disease is provided, the advantages and limitations of mouse, rat, and rabbit models used to mimic pneumonia, sepsis, and meningitis are discussed, and a section on otitis media models is also included. The choice of appropriate animal models for in vivo studies is a key element for improved understanding of pneumococcal disease.

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Dessing, Mark C., Alex F. de Vos, Sandrine Florquin, and Tom van der Poll. "Monocyte Chemoattractant Protein 1 Does Not Contribute to Protective Immunity against Pneumococcal Pneumonia." Infection and Immunity 74, no. 12 (September 18, 2006): 7021–23. http://dx.doi.org/10.1128/iai.00977-06.

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ABSTRACT To determine the role of monocyte chemoattractant protein 1 (MCP-1) during pneumococcal pneumonia, MCP-1 knockout and wild-type mice were infected with Streptococcus pneumoniae. Pulmonary MCP-1 levels were strongly correlated to bacterial loads in wild-type mice. However, MCP-1 knockout and wild-type mice were indistinguishable with respect to bacterial growth, inflammatory responses, and lethality.

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23

Blondeau, Joseph M., and Thomas J. Marrie. "Immunoblotting is of no value in the serodiagnosis of Streptococcus pneumoniae pneumonia." Serodiagnosis and Immunotherapy in Infectious Disease 4, no. 4 (August 1990): 317–28. http://dx.doi.org/10.1016/0888-0786(90)90020-o.

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Ibrahim, Yasser Musa, Alison R. Kerr, Jackie McCluskey, and Tim J. Mitchell. "Role of HtrA in the Virulence and Competence of Streptococcus pneumoniae." Infection and Immunity 72, no. 6 (June 2004): 3584–91. http://dx.doi.org/10.1128/iai.72.6.3584-3591.2004.

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ABSTRACT HtrA is a major virulence factor of Streptococcus pneumoniae (the pneumococcus). Deletion of the gene for HtrA from strain D39 of the pneumococcus completely abolished its virulence in mouse models of pneumonia and bacteremia, while the virulence of a second strain (TIGR4) was dramatically reduced. HtrA-negative mutants induced much less inflammation in the lungs during pneumonia than the wild type. HtrA is involved in the ability of the pneumococcus to grow at high temperatures, to resist oxidative stress, and to undergo genetic transformation. The expression and cellular location of several known virulence factors of the pneumococcus were not affected by the lack of HtrA.

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Portenko, S. A., E. S. Kazakova, E. V. Naidenova, N. A. Osina, M. V. Proskuriakova, A. D. Katyshev, E. A. Sharkova, et al. "Etiological pattern of community-acquired pneumonia related to the new coronavirus infection COVID-19 pandemic in the Saratov Region." Russian Journal of Infection and Immunity 12, no. 1 (December 15, 2021): 95–104. http://dx.doi.org/10.15789/2220-7619-epo-1747.

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Community-acquired pneumonia is a polyetiological infectious disease of bacterial or viral nature. In most cases, it is caused by pathogens such as Streptococcus pneumoniae, Mycoplasma pneumoniae, Haemophilus influenzae, Chlamydophila pneumoniae, Staphylococcus aureus, Legionella spp. However, despite that a wide range of modern diagnostic methods have been introduced into laboratory practice, the etiology of the disease can be determined only in 40–60% of cases. Here, we analyzed the causative agents of community-acquired pneumonia and relevant markers samples of clinical material collected from patients undergoing treatment in the medical facilities of the city of Saratov and the Saratov Region during the period from July to August, 2020, coupled to increase number of cases of new coronavirus infection COVID-19. Clinical material (oropharyngeal swabs, saliva, sputum, blood and blood serum) was obtained from 129 patients and investigated by using microbiological, immunoserological and molecular genetic methods. For this, there were used transport and nutrient media, diagnostic drugs, reagents, discs with antibacterial domestic and foreign drugs registered in the Russian Federation. As a result, 82 (63.6%) patients were found to have markers of the pathogen COVID-19 (viral RNA or specific antibodies of IgM and/or IgG classes), whereas 42% of cases had overlapped RT-PCR and ELISA data. There was a predominance of severe clinical forms of the disease in the group of patients with pneumonia caused by SARS-CoV-2 virus (17.1%), compared with pneumonia of another etiology (12.8%). No marked differences in specific pattern of the accompanying microflora and its sensitivity to antibacterial agents were observed in persons with/without markers of COVID-19. While being examined by bacteriological methods, S. aureus, K. pneumoniae, S. pneumoniae, M. pneumoniae, Acinetobacter spp., both in monoculture and in associations, were isolated from samples of clinical material collected from the majority of patients. In 49.6% of cases, pathogenic microflora, including pathogens causing community-acquired pneumonia, has not been identified, which may be due to the use of antibacterial drugs before the collection of clinical material and treatment applied due to comorbid chronic diseases.

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Pimenta, F. C., E. N. Miyaji, A. P. M. Arêas, M. L. S. Oliveira, A. L. S. S. de Andrade, P. L. Ho, S. K. Hollingshead, and L. C. C. Leite. "Intranasal Immunization with the Cholera Toxin B Subunit-Pneumococcal Surface Antigen A Fusion Protein Induces Protection against Colonization with Streptococcus pneumoniae and Has Negligible Impact on the Nasopharyngeal and Oral Microbiota of Mice." Infection and Immunity 74, no. 8 (August 2006): 4939–44. http://dx.doi.org/10.1128/iai.00134-06.

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ABSTRACT One of the candidate proteins for a mucosal vaccine antigen against Streptococcus pneumoniae is PsaA (pneumococcal surface antigen A). Vaccines targeting mucosal immunity may raise concerns as to possible alterations in the normal microbiota, especially in the case of PsaA, which was shown to have homologs with elevated sequence identity in other viridans group streptococci. In this work, we demonstrate that intranasal immunization with a cholera toxin B subunit-PsaA fusion protein is able to protect mice against colonization with S. pneumoniae but does not significantly alter the natural oral or nasopharyngeal microbiota of mice.

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Peng, Yang, Xiaofang Wang, Hong Wang, Wenchun Xu, Kaifeng Wu, Xuemei Go, Yibing Yin, and Xuemei Zhang. "Interleukin‐4 protects mice against lethal influenza and Streptococcus pneumoniae co‐infected pneumonia." Clinical & Experimental Immunology 205, no. 3 (July 7, 2021): 379–90. http://dx.doi.org/10.1111/cei.13628.

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Parker, Dane, Grace Soong, Paul Planet, Jonathan Brower, Adam J. Ratner, and Alice Prince. "The NanA Neuraminidase of Streptococcus pneumoniae Is Involved in Biofilm Formation." Infection and Immunity 77, no. 9 (June 29, 2009): 3722–30. http://dx.doi.org/10.1128/iai.00228-09.

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ABSTRACT Streptococcus pneumoniae remains a major cause of bacteremia, pneumonia, and otitis media despite vaccines and effective antibiotics. The neuraminidase of S. pneumoniae, which catalyzes the release of terminal sialic acid residues from glycoconjugates, is involved in host colonization in animal models of infection and may provide a novel target for preventing pneumococcal infection. We demonstrate that the S. pneumoniae neuraminidase (NanA) cleaves sialic acid and show that it is involved in biofilm formation, suggesting an additional role in pathogenesis, and that it shares this property with the neuraminidase of Pseudomonas aeruginosa even though we show that the two enzymes are phylogenetically divergent. Using an in vitro model of biofilm formation incorporating human airway epithelial cells, we demonstrate that small-molecule inhibitors of NanA block biofilm formation and may provide a novel target for preventative therapy. This work highlights the role played by the neuraminidase in pathogenesis and represents an important step in drug development for prevention of colonization of the respiratory tract by this important pathogen.

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Wilén, Maria, William Buwembo, Hakim Sendagire, Fred Kironde, and Göte Swedberg. "Cotrimoxazole resistance of Streptococcus pneumoniae and commensal streptococci from Kampala, Uganda." Scandinavian Journal of Infectious Diseases 41, no. 2 (January 2009): 113–21. http://dx.doi.org/10.1080/00365540802651889.

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30

Sopena, Nieves, Maria Luisa Pedro-botet, Miquel Sabrià, Delia García-parés, Esteban Reynaga, and Marian García-nuñez. "Comparative Study of Community-Acquired Pneumonia Caused by Streptococcus pneumoniae, Legionella pneumophila or Chlamydia pneumoniae." Scandinavian Journal of Infectious Diseases 36, no. 5 (May 2004): 330–34. http://dx.doi.org/10.1080/00365540410020091.

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31

Kartashova, N. P., I. A. Leneva, I. N. Falynskova, and A. V. Poddubikov. "Examining effects of NS1 specific antibodies on sublethal influenza infection and secondary bacterial pneumonia in mice." Russian Journal of Immunology 23, no. 4 (October 15, 2020): 383–88. http://dx.doi.org/10.46235/1028-7221-438-eeo.

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Influenza is a highly contagious respiratory disease widespread throughout the world that causes disease in humans, birds and many mammalian species. Annually, around 20% of the global human gets sick with influenza so that more than 500,000 people die its various complications. Secondary bacterial pneumonia poses the peak threat during influenza infection, being most frequently caused by S. pneumoniae. Multiple studies in humans confirm the negative impact of influenza virus infection on subsequent outcome of bacterial pneumonia and provides insight into increased morbidity and mortality due to complicated influenza infection. In particular, the last 2009 influenza pandemic caused by H1N1 virus revealed that 25-56% cases of severe disease forms were associated with secondary pneumonia, among which 14-46% of them were fatal. Based on the aforementioned, it is of high priority to investigate a role of influenza virus proteins in developing of pathogen synergism in viral-bacterial pneumonia, particularly influenza virus non-structural protein NS1. The study objective was to examine effects of NS1-specific antibodies on course of influenza infection and secondary bacterial pneumonia in mice. For this, we used an experimental model of sublethal influenza infection followed by secondary Streptococcus pneumoniae bacterial pneumonia. Influenza A/Puerto Rico/8/34 (H1N1) virus and S. pneumoniae No. 3405 strain were used to simulate influenza infection. Rabbit serum containing antibodies against recombinant NS1 protein from A/Puerto Rico/8/34 virus and native rabbit serum (contain no specific antibodies) were used for vaccination. The study was carried out with female BALB/c mice, weighing 20-22 g. Protective activity of animal serum was assessed by using the three criteria: infection-related mortality, life expectancy and body weight change. The data obtained showed that passive transfer of antibodies specific to influenza virus NS1 protein did not lowered viral replication in sublethal murine model of influenza infection. Subsequent secondary bacterial pneumonia induced by S. pneumoniae revealed no protective effect of anti-NS1 protein antibodies assessed by measuring survival rate, lung viral and bacterial titers in treated vs. control mice.

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Jagdmann, Sandra, Claudia Dames, Daniel Berchtold, Katarzyna Winek, Luis Weitbrecht, Andreas Meisel, and Christian Meisel. "Impact of Key Nicotinic AChR Subunits on Post-Stroke Pneumococcal Pneumonia." Vaccines 8, no. 2 (May 28, 2020): 253. http://dx.doi.org/10.3390/vaccines8020253.

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Pneumonia is the most frequent severe medical complication after stroke. An overactivation of the cholinergic signaling after stroke contributes to immunosuppression and the development of spontaneous pneumonia caused by Gram-negative pathogens. The α7 nicotinic acetylcholine receptor (α7nAChR) has already been identified as an important mediator of the anti-inflammatory pathway after stroke. However, whether the α2, α5 and α9/10 nAChR expressed in the lung also play a role in suppression of pulmonary innate immunity after stroke is unknown. In the present study, we investigate the impact of various nAChRs on aspiration-induced pneumonia after stroke. Therefore, α2, α5, α7 and α9/10 nAChR knockout (KO) mice and wild type (WT) littermates were infected with Streptococcus pneumoniae (S. pneumoniae) three days after middle cerebral artery occlusion (MCAo). One day after infection pathogen clearance, cellularity in lung and spleen, cytokine secretion in bronchoalveolar lavage (BAL) and alveolar-capillary barrier were investigated. Here, we found that deficiency of various nAChRs does not contribute to an enhanced clearance of a Gram-positive pathogen causing post-stroke pneumonia in mice. In conclusion, these findings suggest that a single nAChR is not sufficient to mediate the impaired pulmonary defense against S. pneumoniae after experimental stroke.

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Mina, M. "Streptococcus pneumoniae and viruses in the nasopharynx: Interactions and immunologic responses." International Journal of Infectious Diseases 16 (June 2012): e31. http://dx.doi.org/10.1016/j.ijid.2012.05.082.

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34

Mizgerd, Joseph P., Hiroshi Kubo, Gregory J. Kutkoski, Sabrina D. Bhagwan, Karin Scharffetter-Kochanek, Arthur L. Beaudet, and Claire M. Doerschuk. "Neutrophil Emigration in the Skin, Lungs, and Peritoneum: Different Requirements for CD11/CD18 Revealed by CD18-deficient Mice." Journal of Experimental Medicine 186, no. 8 (October 20, 1997): 1357–64. http://dx.doi.org/10.1084/jem.186.8.1357.

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To determine the role of CD11/CD18 complexes in neutrophil emigration, inflammation was induced in the skin, lungs, or peritoneum of mutant mice deficient in CD18 (CD18−/− mutants). Peripheral blood of CD18−/− mutants contained 11-fold more neutrophils than did blood of wild-type (WT) mice. During irritant dermatitis induced by topical application of croton oil, the number of emigrated neutrophils in histological sections of dermis was 98% less in CD18−/− mutants than in WT mice. During Streptococcus pneumoniae pneumonia, neutrophil emigration in CD18−/− mutants was not reduced. These data are consistent with expectations based on studies using blocking antibodies to inhibit CD11/CD18 complexes, and on observations of humans lacking CD11/CD18 complexes. The number of emigrated neutrophils in lung sections during Escherichia coli pneumonia, or in peritoneal lavage fluid after 4 h of S. pneumoniae peritonitis, was not reduced in CD18−/− mutants, but rather was greater than the WT values (240 ± 30 and 220 ± 30% WT, respectively). Also, there was no inhibition of neutrophil emigration during sterile peritonitis induced by intraperitoneal injection of thioglycollate (90 ± 20% WT). These data contrast with expectations. Whereas CD11/CD18 complexes are essential to the dermal emigration of neutrophils during acute dermatitis, CD18−/− mutant mice demonstrate surprising alternative pathways for neutrophil emigration during pneumonia or peritonitis.

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Kaplan, Sheldon L., and Edward O. Mason. "Management of Infections Due to Antibiotic-Resistant Streptococcus pneumoniae." Clinical Microbiology Reviews 11, no. 4 (October 1, 1998): 628–44. http://dx.doi.org/10.1128/cmr.11.4.628.

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SUMMARY Antibiotic-resistant strains of Streptococcus pneumoniae are becoming more prevalent throughout the world; this has resulted in modifications of treatment approaches. Management of bacterial meningitis has the greatest consensus. Strategies for treating other systemic infections such as pneumonia, bacteremia, and musculoskeletal infections are evolving, in part related to the availability of new antibiotics which are active in vitro against isolates resistant to penicillin and the extended-spectrum cephalosporins. However, there are currently very limited data related to the clinical efficacy of these new agents. The studies upon which current recommendations are based are reviewed. Otitis media represents the single most common infection due to S. pneumoniae. Recommendations for treatment of acute otitis media due to drug-resistant strains and the rationale for these recommendations are discussed.

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Poulsen, Knud, Jesper Reinholdt, Christina Jespersgaard, Kit Boye, Thomas A. Brown, Majbritt Hauge, and Mogens Kilian. "A Comprehensive Genetic Study of Streptococcal Immunoglobulin A1 Proteases: Evidence for Recombination within and between Species." Infection and Immunity 66, no. 1 (January 1, 1998): 181–90. http://dx.doi.org/10.1128/iai.66.1.181-190.1998.

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ABSTRACT An analysis of 13 immunoglobulin A1 (IgA1) protease genes (iga) of strains of Streptococcus pneumoniae,Streptococcus oralis, Streptococcus mitis, andStreptococcus sanguis was carried out to obtain information on the structure, polymorphism, and phylogeny of this specific protease, which enables bacteria to evade functions of the predominant Ig isotype on mucosal surfaces. The analysis included cloning and sequencing of iga genes from S. oralisand S. mitis biovar 1, sequencing of an additional seveniga genes from S. sanguis biovars 1 through 4, and restriction fragment length polymorphism (RFLP) analyses of iga genes of another 10 strains of S. mitisbiovar 1 and 6 strains of S. oralis. All 13 genes sequenced had the potential of encoding proteins with molecular masses of approximately 200 kDa containing the sequence motif HEMTH and an E residue 20 amino acids downstream, which are characteristic of Zn metalloproteinases. In addition, all had a typical gram-positive cell wall anchor motif, LPNTG, which, in contrast to such motifs in other known streptococcal and staphylococcal proteins, was located in their N-terminal parts. Repeat structures showing variation in number and sequence were present in all strains and may be of relevance to the immunogenicities of the enzymes. Protease activities in cultures of the streptococcal strains were associated with species of different molecular masses ranging from 130 to 200 kDa, suggesting posttranslational processing possibly as a result of autoproteolysis at post-proline peptide bonds in the N-terminal parts of the molecules. Comparison of deduced amino acid sequences revealed a 94% similarity between S. oralis and S. mitis IgA1 proteases and a 75 to 79% similarity between IgA1 proteases of these species and those of S. pneumoniae and S. sanguis, respectively. Combined with the results of RFLP analyses using different iga gene fragments as probes, the results of nucleotide sequence comparisons provide evidence of horizontal transfer of iga gene sequences among individual strains of S. sanguis as well as among S. mitis and the two speciesS. pneumoniae and S. oralis. Whileiga genes of S. sanguis and S. oralis were highly homogeneous, the genes of S. pneumoniae and S. mitis showed extensive polymorphism reflected in different degrees of antigenic diversity.

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Marks, Laura R., Ryan M. Reddinger, and Anders P. Hakansson. "Biofilm Formation Enhances Fomite Survival of Streptococcus pneumoniae and Streptococcus pyogenes." Infection and Immunity 82, no. 3 (December 26, 2013): 1141–46. http://dx.doi.org/10.1128/iai.01310-13.

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ABSTRACTBothStreptococcus pyogenesandStreptococcus pneumoniaeare widely thought to rapidly die outside the human host, losing infectivity following desiccation in the environment. However, to date, all literature investigating the infectivity of desiccated streptococci has used broth-grown, planktonic populations. In this study, we examined the impact of biofilm formation on environmental survival of clinical and laboratory isolates ofS. pyogenesandS. pneumoniaeas both organisms are thought to colonize the human host as biofilms. Results clearly demonstrate that while planktonic cells that are desiccated rapidly lose viability both on hands and abiotic surfaces, such as plastic, biofilm bacteria remain viable over extended periods of time outside the host and remain infectious in a murine colonization model. To explore the level and extent of streptococcal fomite contamination that children might be exposed to naturally, direct bacteriologic cultures of items in a day care center were conducted, which demonstrated high levels of viable streptococci of both species. These findings raise the possibility that streptococci may survive in the environment and be transferred from person to person via fomites contaminated with oropharyngeal secretions containing biofilm streptococci.

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Whatmore, Adrian M., Androulla Efstratiou, A. Paul Pickerill, Karen Broughton, Geoffrey Woodard, Daniel Sturgeon, Robert George, and Christopher G. Dowson. "Genetic Relationships between Clinical Isolates of Streptococcus pneumoniae, Streptococcus oralis, and Streptococcus mitis: Characterization of “Atypical” Pneumococci and Organisms Allied to S. mitis HarboringS. pneumoniae Virulence Factor-Encoding Genes." Infection and Immunity 68, no. 3 (March 1, 2000): 1374–82. http://dx.doi.org/10.1128/iai.68.3.1374-1382.2000.

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ABSTRACT The oral streptococcal group (mitis phylogenetic group) currently consists of nine recognized species, although the group has been traditionally difficult to classify, with frequent changes in nomenclature over the years. The pneumococcus (Streptococcus pneumoniae), an important human pathogen, is traditionally distinguished from the most closely related oral streptococcal speciesStreptococcus mitis and Streptococcus oralis on the basis of three differentiating characteristics: optochin susceptibility, bile solubility, and agglutination with antipneumococcal polysaccharide capsule antibodies. However, there are many reports in the literature of pneumococci lacking one or more of these defining characteristics. Sometimes called “atypical” pneumococci, these isolates can be the source of considerable confusion in the clinical laboratory. Little is known to date about the genetic relationships of such organisms with classical S. pneumoniae isolates. Here we describe these relationships based on sequence analysis of housekeeping genes in comparison with previously characterized isolates of S. pneumoniae,S. mitis, and S. oralis. While most pneumococci were found to represent a closely related group these studies identified a subgroup of atypical pneumococcal isolates (bile insoluble and/or “acapsular”) distinct from, though most closely related to, the “typical” pneumococcal isolates. However, a large proportion of isolates, found to be atypical on the basis of capsule reaction alone, did group with typical pneumococci, suggesting that they have either lost capsule production or represent as-yet-unrecognized capsular types. In contrast to typical S. pneumoniae, isolates phenotypically identified as S. mitis and S. oralis, which included isolates previously characterized in taxonomic studies, were genetically diverse. While most of the S. oralis isolates did fall into a well-separated group, S. mitis isolates did not cluster into a well-separated group. During the course of these studies we also identified a number of potentially important pathogenic isolates, which were frequently associated with respiratory disease, that phenotypically and genetically are most closely related to S. mitis but which harbor genes encoding the virulence determinants pneumolysin and autolysin classically associated with S. pneumoniae.

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Jado, Isabel, Asunción Fenoll, Julio Casal, and Amalia Pérez. "Identification of the psaA Gene, Coding for Pneumococcal Surface Adhesin A, in Viridans Group Streptococci other than Streptococcus pneumoniae." Clinical Diagnostic Laboratory Immunology 8, no. 5 (September 1, 2001): 895–98. http://dx.doi.org/10.1128/cdli.8.5.895-898.2001.

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ABSTRACT The gene encoding the pneumococcal surface adhesin A (PsaA) protein has been identified in three different viridans group streptococcal species. Comparative studies of the psaA gene identified in different pneumococcal isolates by sequencing PCR products showed a high degree of conservation among these strains. PsaA is encoded by an open reading frame of 930 bp. The analysis of this fragment inStreptococcus mitis, Streptococcus oralis, andStreptococcus anginosus strains revealed a sequence identity of 95, 94, and 90%, respectively, to the corresponding open reading frame of the previously reported Streptococcus pneumoniae serotype 6B strain. Our results confirm thatpsaA is present and detectable in heterologous bacterial species. The possible implications of these results for the suitability and potential use of PsaA in the identification and diagnosis of pneumococcal diseases are discussed.

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Dunlap, W., J. R. Baker, J. Knowlton, P. Makidon, and N. Mank. "A Novel Streptococcus pneumoniae Vaccine." Journal of Allergy and Clinical Immunology 125, no. 2 (February 2010): AB78. http://dx.doi.org/10.1016/j.jaci.2009.12.304.

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Herrmann, Isabel, Markus Kellert, Hauke Schmidt, Alexander Mildner, Uwe K. Hanisch, Wolfgang Brück, Marco Prinz, and Roland Nau. "Streptococcus pneumoniae Infection Aggravates Experimental Autoimmune Encephalomyelitis via Toll-Like Receptor 2." Infection and Immunity 74, no. 8 (August 2006): 4841–48. http://dx.doi.org/10.1128/iai.00026-06.

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ABSTRACT The course of autoimmune inflammatory diseases of the central nervous system (CNS) can be influenced by infections. Here we assessed the disease-modulating effects of the most frequent respiratory pathogen Streptococcus pneumonia on the course of experimental autoimmune encephalomyelitis (EAE). Mice were immunized with myelin oligodendrocyte glycoprotein 35-55 (MOG35-55) peptide, challenged intraperitoneally with live S. pneumoniae type 3, and then treated with ceftriaxone. EAE was monitored by a clinical score for 35 days after immunization. EAE was unaltered in mice infected with S. pneumoniae 2 days before and 21 days after the first MOG35-55 injection but was more severe in animals infected 7 days after the first MOG35-55 injection. The antigen-driven systemic T-cell response was unaltered, and the intraspinal Th1 cytokine mRNA concentrations at the peak of disease were unchanged. The composition of CNS-infiltrating cells and subsequent tissue destruction were only slightly increased after S. pneumoniae infection. In contrast, the serum levels of tumor necrosis factor alpha and interleukin-6 and spinal interleukin-6 levels were elevated, and the expression of major histocompatibility complex class II molecules, CD80, and CD86 on splenic dendritic cells were enhanced early after infection. Serum cytokine concentrations were not elevated, and EAE was not aggravated by S. pneumoniae infection in Toll-like receptor 2 (TLR2)-deficient mice. In conclusion, infection with S. pneumoniae worsens EAE probably by elevation of proinflammatory cytokines and activation of dendritic cells in the systemic circulation via TLR2 and cross talk through the blood-brain barrier.

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CATCHPOLE, C., A. FRAISE, and R. WISE. "Multidrug-Resistant Streptococcus pneumoniae." Microbial Drug Resistance 2, no. 4 (January 1996): 431–32. http://dx.doi.org/10.1089/mdr.1996.2.431.

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Masomian, Malihe, Zuleeza Ahmad, Lai Ti Gew, and Chit Laa Poh. "Development of Next Generation Streptococcus pneumoniae Vaccines Conferring Broad Protection." Vaccines 8, no. 1 (March 17, 2020): 132. http://dx.doi.org/10.3390/vaccines8010132.

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Streptococcus pneumoniae is a major pathogen causing pneumonia with over 2 million deaths annually, especially in young children and the elderly. To date, at least 98 different pneumococcal capsular serotypes have been identified. Currently, the vaccines for prevention of S. pneumoniae infections are the 23-valent pneumococcal polysaccharide-based vaccine (PPV23) and the pneumococcal conjugate vaccines (PCV10 and PCV13). These vaccines only cover some pneumococcal serotypes and are unable to protect against non-vaccine serotypes and unencapsulated S. pneumoniae. This has led to a rapid increase in antibiotic-resistant non-vaccine serotypes. Hence, there is an urgent need to develop new, effective, and affordable pneumococcal vaccines, which could cover a wide range of serotypes. This review discusses the new approaches to develop effective vaccines with broad serotype coverage as well as recent development of promising pneumococcal vaccines in clinical trials. New vaccine candidates are the inactivated whole-cell vaccine strain (Δpep27ΔcomD mutant) constructed by mutations of specific genes and several protein-based S. pneumoniae vaccines using conserved pneumococcal antigens, such as lipoprotein and surface-exposed protein (PspA). Among the vaccines in Phase 3 clinical trials are the pneumococcal conjugate vaccines, PCV-15 (V114) and 20vPnC. The inactivated whole-cell and several protein-based vaccines are either in Phase 1 or 2 trials. Furthermore, the recent progress of nanoparticles that play important roles as delivery systems and adjuvants to improve the performance, as well as the immunogenicity of the nanovaccines, are reviewed.

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Ulanova, M., V. Tatochenko, and L. Katosova. "Correlation between the immune response to streptococcus pneumoniae and pneumonia morbidity in children." Tubercle and Lung Disease 75 (June 1994): 93. http://dx.doi.org/10.1016/0962-8479(94)91027-8.

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Popova, A. Yu, E. B. Ezhlova, Yu V. Demina, A. K. Noskov, E. V. Kovalev, O. S. Chemisova, T. I. Tverdokhlebova, et al. "Features of Etiology of Community-Acquired Pneumonia Associated with COVID-19." Problems of Particularly Dangerous Infections, no. 4 (February 7, 2021): 99–105. http://dx.doi.org/10.21055/0370-1069-2020-4-99-105.

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Objective: comparative study of the etiological structure of community-acquired pneumonia in SARSCoV-2 “+”and SARS-CoV-2 “-“ patients who sought help from medical organizations in the Rostov Region.Materials and methods. Biological material from 508 patients diagnosed with community-acquired pneumonia who were on outpatient treatment or in hospitals in Rostov-on-Don was studied. Verification of respiratory viruses, including SARS-CoV-2 RNA, as well as M. pneumoniae, C. pneumoniae, and L. pneumophila was performed by polymerase chain reaction in nasopharyngeal smears. Bacteriological analysis of sputum was carried out using differential diagnostic media, identification of isolated pathogens was carried out using time-of-flight mass spectrometry on Autoflex (Bruker Daltonics) with BioTyper 3.0 software.Results and discussion. During the spread of a new coronavirus infection in the Rostov Region, the main etiological agent of community-acquired pneumonia is the new SARS-CoV-2 coronavirus. Specific character of pneumonia in patients with laboratory-confirmed COVID-19 is a higher incidence of mixed infection of both viral and bacterial etiology. Against the background of detection of a new coronavirus infection in patients with pneumonia, cases of detection of other types of coronaviruses have been registered (HKU-1,OC43, HL-63 and 229Е). The most common etiological agent of bacterial pneumonia in patients was Streptococcus spp., both in patients with COVID-19-associated pneumonia and in patients who tested negative for SARS-CoV-2. Coronavirus patients represent a high risk group for the development of mycotic lung lesions.

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Kerr, Alison R., Gavin K. Paterson, Alan Riboldi-Tunnicliffe, and Tim J. Mitchell. "Innate Immune Defense against Pneumococcal Pneumonia Requires Pulmonary Complement Component C3." Infection and Immunity 73, no. 7 (July 2005): 4245–52. http://dx.doi.org/10.1128/iai.73.7.4245-4252.2005.

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ABSTRACT Complement is known to be involved in protection against systemic infection with Streptococcus pneumoniae. However, less is known about effects of complement within the lungs during pneumococcal pneumonia. By intranasally infecting transgenic mice unable to express complement C3, we investigated the role of complement in pulmonary defenses against S. pneumoniae. It was demonstrated that within the lungs, there is a requirement for C3 during the initial hours of infection. It was found that within 1 h of infection, bacterial loads decreased within lung airways of control mice as C3 protein increased. The lack of C3 resulted in the inability to control growth of wild-type or attenuated pneumococci within the lungs and bloodstream, resulting in an overwhelming inflammatory response and shorter survival times. Our results show that during the initial hours of infection with S. pneumoniae, C3 is protective within the lungs and subsequently plays an important role systemically.

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Neth, Olaf, Dominic L. Jack, Alister W. Dodds, Helen Holzel, Nigel J. Klein, and Malcolm W. Turner. "Mannose-Binding Lectin Binds to a Range of Clinically Relevant Microorganisms and Promotes Complement Deposition." Infection and Immunity 68, no. 2 (February 1, 2000): 688–93. http://dx.doi.org/10.1128/iai.68.2.688-693.2000.

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ABSTRACT Mannose-binding lectin (MBL) is a collagenous serum lectin believed to be of importance in innate immunity. Genetically determined low levels of the protein are known to predispose to infections. In this study the binding of purified MBL to pathogens isolated from immunocompromised children was investigated by flow cytometry. DiverseCandida species, Aspergillus fumigatus,Staphylococcus aureus, and beta-hemolytic group A streptococci exhibited strong binding of MBL, whereas Escherichia coli, Klebsiella species, and Haemophilus influenzae type b were characterized by heterogeneous binding patterns. In contrast, beta-hemolytic group B streptococci,Streptococcus pneumoniae, and Staphylococcus epidermidis showed low levels of binding. Bound MBL was able to promote C4 deposition in a concentration-dependent manner. We conclude that MBL may be of importance in first-line immune defense against several important pathogens.

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Whatmore, Adrian M., Samantha J. King, Neil C. Doherty, Daniel Sturgeon, Neil Chanter, and Christopher G. Dowson. "Molecular Characterization of Equine Isolates ofStreptococcus pneumoniae: Natural Disruption of Genes Encoding the Virulence Factors Pneumolysin and Autolysin." Infection and Immunity 67, no. 6 (June 1, 1999): 2776–82. http://dx.doi.org/10.1128/iai.67.6.2776-2782.1999.

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ABSTRACT Although often considered a strict human pathogen,Streptococcus pneumoniae has been reported to infect and cause pneumonia in horses, although the pathology appears restricted compared to that of human infections. Here we report on the molecular characterization of a group of S. pneumoniae isolates obtained from horses in England and Ireland. Despite being obtained from geographically distinct locations, the isolates were found to represent a tight clonal group, virtually identical to each other but genetically distinguishable from more than 120 divergent isolates of human S. pneumoniae. A comprehensive analysis of known pneumococcal virulence determinants was undertaken in an attempt to understand the pathogenicity of equine pneumococci. Surprisingly, equine isolates appear to lack activities associated with both the hemolytic cytotoxin pneumolysin, often considered a major virulence factor of pneumococci, and the major autolysin gene lytA, also considered an important virulence factor. In support of phenotypic data, molecular studies demonstrated a deletion of parts of the coding sequences of both lytA and ply genes in equine pneumococci. The implications of these findings for the evolution and pathogenicity of equine S. pneumoniae are discussed.

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Rijneveld, Anita W., Sebastiaan Weijer, Sandrine Florquin, Charles T. Esmon, Joost C. M. Meijers, Peter Speelman, Pieter H. Reitsma, Hugo Ten Cate, and Tom van der Poll. "Thrombomodulin mutant mice with a strongly reduced capacity to generate activated protein C have an unaltered pulmonary immune response to respiratory pathogens and lipopolysaccharide." Blood 103, no. 5 (March 1, 2004): 1702–9. http://dx.doi.org/10.1182/blood-2002-05-1380.

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AbstractThe thrombomodulin–protein C–protein S (TM-PC-PS) pathway exerts anticoagulant and anti-inflammatory effects. We investigated the role of TM in the pulmonary immune response in vivo by the use of mice with a mutation in the TM gene (TMpro/pro) that was earlier found to result in a minimal capacity for activated PC (APC) generation in the circulation. We here demonstrate that TMpro/pro mice also display a strongly reduced capacity to produce APC in the alveolar compartment upon intrapulmonary delivery of PC and thrombin. We monitored procoagulant and inflammatory changes in the lung during Gram-positive (Streptococcus pneumoniae) and Gram-negative (Klebsiella pneumoniae) pneumonia and after local administration of lipopolysaccharide (LPS). Bacterial pneumonia was associated with fibrin(ogen) depositions in the lung that colocalized with inflammatory infiltrates. LPS also induced a rise in thrombin-antithrombin complexes in bronchoalveolar lavage fluid. These pulmonary procoagulant responses were unaltered in TMpro/pro mice, except for enhanced fibrin(ogen) deposition during pneumococcal pneumonia. In addition, TMpro/pro mice displayed unchanged antibacterial defense, neutrophil recruitment, and cytokine/chemokine levels. These data suggest that the capacity of TM to generate APC does not play a role of importance in the pulmonary response to respiratory pathogens or LPS.

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Paudel, Sagar, Pankaj Baral, Laxman Ghimire, Scott Bergeron, Liliang Jin, Joseph A. DeCorte, John T. Le, Shanshan Cai, and Samithamby Jeyaseelan. "CXCL1 regulates neutrophil homeostasis in pneumonia-derived sepsis caused by Streptococcus pneumoniae serotype 3." Blood 133, no. 12 (March 21, 2019): 1335–45. http://dx.doi.org/10.1182/blood-2018-10-878082.

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Abstract Neutrophil migration to the site of bacterial infection is a critical step in host defense. Exclusively produced in the bone marrow, neutrophil release into the blood is tightly controlled. Although the chemokine CXCL1 induces neutrophil influx during bacterial infections, its role in regulating neutrophil recruitment, granulopoiesis, and neutrophil mobilization in response to lung infection-induced sepsis is unclear. Here, we used a murine model of intrapulmonary Streptococcus pneumoniae infection to investigate the role of CXCL1 in host defense, granulopoiesis, and neutrophil mobilization. Our results demonstrate that CXCL1 augments neutrophil influx to control bacterial growth in the lungs, as well as bacterial dissemination, resulting in improved host survival. This was shown in Cxcl1−/− mice, which exhibited defective amplification of early neutrophil precursors in granulocytic compartments, and CD62L- and CD49d-dependent neutrophil release from the marrow. Administration of recombinant CXCL2 and CXCL5 after infection rescues the impairments in neutrophil-dependent host defense in Cxcl1−/− mice. Taken together, these findings identify CXCL1 as a central player in host defense, granulopoiesis, and mobilization of neutrophils during Gram-positive bacterial pneumonia-induced sepsis.

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