Moxifloxacin modulates inflammation during murine pneumonia

Beißwenger, Christoph; Honecker, Anja; Kamyschnikow, Andreas; Bischoff, Markus; Tschernig, Thomas; Bals, Robert

doi:10.1186/1465-9921-15-82

Cited by 20 publications

(20 citation statements)

References 29 publications

(43 reference statements)

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“…The inflammatory score was calculated as described previously (6). Primary antibodies for TNF-␣ (Abcam, UK) were used for immunohistochemistry analysis by a blinded investigator as described previously (32). Seven to 10 fields per lung were evaluated for TNF-␣-positive cells.…”

Section: Methodsmentioning

confidence: 99%

Interleukin 17 Receptor E (IL-17RE) and IL-17C Mediate the Recruitment of Neutrophils during Acute Streptococcus pneumoniae Pneumonia

et al. 2019

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Neutrophils contribute to lung injury in acute pneumococcal pneumonia. The interleukin 17 receptor E (IL-17RE) is the functional receptor for the epithelial-derived cytokine IL-17C, which is known to mediate innate immune functions. The aim of this study was to investigate the contribution of IL-17RE/IL-17C to pulmonary inflammation in a mouse model of acute Streptococcus pneumoniae pneumonia. Numbers of neutrophils and the expression levels of the cytokine granulocyte colony-stimulating factor (G-CSF) and tumor necrosis factor alpha (TNF-α) were decreased in lungs of IL-17RE-deﬁcient (Il-17re−/−) mice infected with S. pneumoniae. Numbers of alveolar macrophages rapidly declined in both wild-type (WT) and Il-17re−/− mice and recovered 72 h after infection. There were no clear differences in the elimination of bacteria and numbers of blood granulocytes between infected WT and Il-17re−/− mice. The fractions of granulocyte-monocyte progenitors (GMPs) were significantly reduced in infected Il-17re−/− mice. Numbers of neutrophils were significantly reduced in lungs of mice deficient for IL-17C 24 h after infection with S. pneumoniae. These data indicate that the IL-17C/IL-17RE axis promotes the recruitment of neutrophils without affecting the recovery of alveolar macrophages in the acute phase of S. pneumoniae lung infection.

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Section: Methodsmentioning

confidence: 99%

Interleukin 17 Receptor E (IL-17RE) and IL-17C Mediate the Recruitment of Neutrophils during Acute Streptococcus pneumoniae Pneumonia

et al. 2019

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“…10,17 The expression of IL-17A was found to be increased in mouse lungs infected with P. aeruginosa. 11,[18][19][20][21] Il-17A-dependent acquired immunity is also required for efficient clearance of Streptococcus pneumoniae in the upper airways. 13,16 Recent studies suggest that IL-17A plays a major role in the pathogenesis of acute respiratory distress syndrome (ARDS).…”

Section: Introductionmentioning

confidence: 99%

IL-17A attracts inflammatory cells in murine lung infection withP. aeruginosa

Wonnenberg

Jungnickel²,

Honecker³

et al. 2016

Innate Immun

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IL-17A-dependent immunity is of importance in the protection against extracellular bacterial pathogens. However, IL-17A is also suggested to mediate the pathogenesis of lung diseases, such as acute respiratory distress syndrome. Here, we studied the role of IL-17A in a mouse model of acute pneumonia. IL-17A mediated the expression of keratinocyte-derived chemokine (KC) and the recruitment of inflammatory cells in mice infected with a sub-lethal dose of Pseudomonas aeruginosa. IL-17A deficiency protected mice from lethal P. aeruginosa lung infection. A sub-lethal infection with Streptococcus pneumoniae resulted in increased bacterial burden associated with increased pulmonary inflammation. Thus, the type of infectious bacteria seemed to influence the way in which IL-17A functions during pulmonary infection. Reducing pulmonary inflammation by targeting IL-17A may be a therapeutic option in acute P. aeruginosa pneumonia.

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“…It inhibits the synthesis of inflammatory mediators and the activation of MAP kinase and NF-kB signaling cascades [11]. In the study of Beisswenger et al [12]showed that moxifloxacin treatment resulted in low levels of pro-inflammatory mediators and neutrophils in the lungs of mice infected with Streptococcus pneumoniae and Pseudomonas aeruginosa. The immunomodulatory effects of moxifloxacin may result in the changes of WBC count like leukopenia with neutropenia at clinically relevant concentrations.…”

Section: Discussionmentioning

confidence: 99%

Moxifloxacin-induced neutropenia in 26-year-old man

Ati̇k

İspir

Aytekin

et al. 2018

J Infect Dev Ctries

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Moxifloxacin is a fourth generation widely used fluoroquinolone antibiotic. There are three cases of moxifloxacin-induced neutropenia reported in the literature and we report the fourth case. A 26-year-old man with pneumonia was treated with moxifloxacin because of penicillin allergy. On the second day of therapy, leukopenia [White blood cell (WBC) count 2.7×10³/μL] and neutropenia (neutrophils 1.21×10³/μL) occurred. Rothia mucilaginosa was isolated in sputum culture. On the fourth day of hospitalization moxifloxacin treatment was stopped and clarithromycin 500 mg PO twice daily was started. Leukopenia and neutropenia resolved one day after discontinuation of moxifloxacin that WBC and neutrophil count rose 4.5×10³/μL and 1.97×10³/μL, respectively. On the sixth day of hospitalization, WBC and neutrophil count was 4.3×10³/μL and 2.29×10³/μL, respectively. The immunomodulatory effects of moxifloxacin may result in the changes of WBC count like leukopenia with neutropenia. Moxifloxacin induced neutropenia may be more common and is an important adverse effect. More observational studies about safety profiles of moxifloxacin are needed.

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Moxifloxacin modulates inflammation during murine pneumonia

Cited by 20 publications

References 29 publications

Interleukin 17 Receptor E (IL-17RE) and IL-17C Mediate the Recruitment of Neutrophils during Acute Streptococcus pneumoniae Pneumonia

Interleukin 17 Receptor E (IL-17RE) and IL-17C Mediate the Recruitment of Neutrophils during Acute Streptococcus pneumoniae Pneumonia

IL-17A attracts inflammatory cells in murine lung infection withP. aeruginosa

Moxifloxacin-induced neutropenia in 26-year-old man

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