tetano
Editor, Senior Moderator
Front Cell Infect Microbiol. 2019 Apr 16;9:108. doi: 10.3389/fcimb.2019.00108. eCollection 2019.
[h=1]Neutrophils Induce a Novel Chemokine Receptors Repertoire During Influenza Pneumonia.[/h] Rudd JM[SUP]1[/SUP], Pulavendran S[SUP]1[/SUP], Ashar HK[SUP]1[/SUP], Ritchey JW[SUP]1[/SUP], Snider TA[SUP]1[/SUP], Malayer JR[SUP]1[/SUP], Marie M[SUP]1[/SUP], Chow VTK[SUP]2[/SUP], Narasaraju T[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Exaggerated host innate immune responses have been implicated in severe influenza pneumonia. We have previously demonstrated that excessive neutrophils recruited during influenza infection drive pulmonary pathology through induction of neutrophil extracellular traps (NETs) and release of extracellular histones. Chemokine receptors (CRs) are essential in the recruitment and activation of leukocytes. Although neutrophils have been implicated in influenza pathogenesis, little is known about their phenotypic changes, including expression of CRs occurring in the infected -lung microenvironment. Here, we examined CC and CXC CRs detection in circulating as well as lung-recruited neutrophils during influenza infection in mice using flow cytometry analyses. Our studies revealed that lung-recruited neutrophils displayed induction of CRs, including CCR1, CCR2, CCR3, CCR5, CXCR1, CXCR3, and CXCR4, all of which were marginally induced in circulating neutrophils. CXCR2 was the most predominant CR observed in both circulating and lung-infiltrated neutrophils after infection. The stimulation of these induced CRs modulated neutrophil phagocytic activity, ligand-specific neutrophil migration, bacterial killing, and NETs induction ex vivo. These findings indicate that neutrophils induce a novel CR repertoire in the infectious lung microenvironment, which alters their functionality during influenza pneumonia.
[h=4]KEYWORDS:[/h] acute lung injury; chemokine receptor; influenza; mouse model; neutrophil
PMID: 31041196 PMCID: PMC6476945 DOI: 10.3389/fcimb.2019.00108
[h=1]Neutrophils Induce a Novel Chemokine Receptors Repertoire During Influenza Pneumonia.[/h] Rudd JM[SUP]1[/SUP], Pulavendran S[SUP]1[/SUP], Ashar HK[SUP]1[/SUP], Ritchey JW[SUP]1[/SUP], Snider TA[SUP]1[/SUP], Malayer JR[SUP]1[/SUP], Marie M[SUP]1[/SUP], Chow VTK[SUP]2[/SUP], Narasaraju T[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Exaggerated host innate immune responses have been implicated in severe influenza pneumonia. We have previously demonstrated that excessive neutrophils recruited during influenza infection drive pulmonary pathology through induction of neutrophil extracellular traps (NETs) and release of extracellular histones. Chemokine receptors (CRs) are essential in the recruitment and activation of leukocytes. Although neutrophils have been implicated in influenza pathogenesis, little is known about their phenotypic changes, including expression of CRs occurring in the infected -lung microenvironment. Here, we examined CC and CXC CRs detection in circulating as well as lung-recruited neutrophils during influenza infection in mice using flow cytometry analyses. Our studies revealed that lung-recruited neutrophils displayed induction of CRs, including CCR1, CCR2, CCR3, CCR5, CXCR1, CXCR3, and CXCR4, all of which were marginally induced in circulating neutrophils. CXCR2 was the most predominant CR observed in both circulating and lung-infiltrated neutrophils after infection. The stimulation of these induced CRs modulated neutrophil phagocytic activity, ligand-specific neutrophil migration, bacterial killing, and NETs induction ex vivo. These findings indicate that neutrophils induce a novel CR repertoire in the infectious lung microenvironment, which alters their functionality during influenza pneumonia.
[h=4]KEYWORDS:[/h] acute lung injury; chemokine receptor; influenza; mouse model; neutrophil
PMID: 31041196 PMCID: PMC6476945 DOI: 10.3389/fcimb.2019.00108