tetano
Editor, Senior Moderator
Zool Res. 2017 May 18;38(3):146-154. doi: 10.24272/j.issn.2095-8137.2017.035.
[h=1]Pulmonary immune cells and inflammatory cytokine dysregulation are associated with mortality of IL-1R1 -/-mice infected with influenza virus (H1N1).[/h] Guo L[SUP]1[/SUP], Wang YC[SUP]1[/SUP], Mei JJ[SUP]2[/SUP], Ning RT[SUP]1[/SUP], Wang JJ[SUP]1[/SUP], Li JQ[SUP]1[/SUP], Wang X[SUP]1[/SUP], Zheng HW[SUP]1[/SUP], Fan HT[SUP]1[/SUP], Liu LD[SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Respirovirus infection can cause viral pneumonia and acute lung injury (ALI). The interleukin-1 (IL-1) family consists of proinflammatory cytokines that play essential roles in regulating immune and inflammatory responses in vivo. IL-1 signaling is associated with protection against respiratory influenza virus infection by mediation of the pulmonary anti-viral immune response and inflammation. We analyzed the infiltration lung immune leukocytes and cytokines that contribute to inflammatory lung pathology and mortality of fatal H1N1 virus-infected IL-1 receptor 1 (IL-1R1) deficient mice. Results showed that early innate immune cells and cytokine/chemokine dysregulation were observed with significantly decreased neutrophil infiltration and IL-6, TNF-α, G-CSF, KC, and MIP-2 cytokine levels in the bronchoalveolar lavage fluid of infected IL-1R1 [SUP]-/-[/SUP] mice in comparison with that of wild type infected mice. The adaptive immune response against the H1N1 virus in IL-1R1 [SUP]-/-[/SUP] mice was impaired with downregulated anti-viral Th1 cell, CD8+ cell, and antibody functions, which contributes to attenuated viral clearance. Histological analysis revealed reduced lung inflammation during early infection but severe lung pathology in late infection in IL-1R1 [SUP]-/-[/SUP] mice compared with that in WT infected mice. Moreover, the infected IL-1R1 [SUP]-/-[/SUP] mice showed markedly reduced neutrophil generation in bone marrow and neutrophil recruitment to the inflamed lung. Together, these results suggest that IL-1 signaling is associated with pulmonary anti-influenza immune response and inflammatory lung injury, particularly via the influence on neutrophil mobilization and inflammatory cytokine/chemokine production.
[h=4]KEYWORDS:[/h] IL-1 receptor 1; Influenza; Lung inflammation; Neutrophil
PMID: 28585438 DOI: 10.24272/j.issn.2095-8137.2017.035
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[h=1]Pulmonary immune cells and inflammatory cytokine dysregulation are associated with mortality of IL-1R1 -/-mice infected with influenza virus (H1N1).[/h] Guo L[SUP]1[/SUP], Wang YC[SUP]1[/SUP], Mei JJ[SUP]2[/SUP], Ning RT[SUP]1[/SUP], Wang JJ[SUP]1[/SUP], Li JQ[SUP]1[/SUP], Wang X[SUP]1[/SUP], Zheng HW[SUP]1[/SUP], Fan HT[SUP]1[/SUP], Liu LD[SUP]3[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Respirovirus infection can cause viral pneumonia and acute lung injury (ALI). The interleukin-1 (IL-1) family consists of proinflammatory cytokines that play essential roles in regulating immune and inflammatory responses in vivo. IL-1 signaling is associated with protection against respiratory influenza virus infection by mediation of the pulmonary anti-viral immune response and inflammation. We analyzed the infiltration lung immune leukocytes and cytokines that contribute to inflammatory lung pathology and mortality of fatal H1N1 virus-infected IL-1 receptor 1 (IL-1R1) deficient mice. Results showed that early innate immune cells and cytokine/chemokine dysregulation were observed with significantly decreased neutrophil infiltration and IL-6, TNF-α, G-CSF, KC, and MIP-2 cytokine levels in the bronchoalveolar lavage fluid of infected IL-1R1 [SUP]-/-[/SUP] mice in comparison with that of wild type infected mice. The adaptive immune response against the H1N1 virus in IL-1R1 [SUP]-/-[/SUP] mice was impaired with downregulated anti-viral Th1 cell, CD8+ cell, and antibody functions, which contributes to attenuated viral clearance. Histological analysis revealed reduced lung inflammation during early infection but severe lung pathology in late infection in IL-1R1 [SUP]-/-[/SUP] mice compared with that in WT infected mice. Moreover, the infected IL-1R1 [SUP]-/-[/SUP] mice showed markedly reduced neutrophil generation in bone marrow and neutrophil recruitment to the inflamed lung. Together, these results suggest that IL-1 signaling is associated with pulmonary anti-influenza immune response and inflammatory lung injury, particularly via the influence on neutrophil mobilization and inflammatory cytokine/chemokine production.
[h=4]KEYWORDS:[/h] IL-1 receptor 1; Influenza; Lung inflammation; Neutrophil
PMID: 28585438 DOI: 10.24272/j.issn.2095-8137.2017.035
Free full text