Interleukin-22 produced by alveolar macrophages during activation of the innate immune response

2013 ◽  
Vol 62 (6) ◽  
pp. 561-569 ◽  
Author(s):  
Marit Hansson ◽  
Elin Silverpil ◽  
Anders Lindén ◽  
Pernilla Glader
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Alveolar Macrophages ◽  
Innate Immune ◽  
Interleukin 22

scholarly journals Respiratory epithelium: Place of entry and / or defense against SARS-CoV-2 virus

Praxis medica ◽  
2021 ◽  
Vol 50 (1-2) ◽  
pp. 35-43
Author(s):  
Snežana Leštarević ◽  
Slađana Savić ◽  
Leonida Vitković ◽  
Predrag Mandić ◽  
Milica Mijović ◽  
...  
Keyword(s):  
Immune Response ◽  
Epithelial Cells ◽  
Innate Immune Response ◽  
Alveolar Macrophages ◽  
Rna Virus ◽  
The Body ◽  
Innate Immune ◽  
Alveolar Epithelial Cells ◽  
Biologically Active ◽  
Lung Damage

Coronavirus Disease (COVID-19) is caused by the RNA virus SARS-CoV-2. The primary receptor for the virus is most likely Angiotensin-converting enzyme 2 (ACE2), and the virus enters the body by infecting epithelial cells of the respiratory tract. Through the activation of Toll Like Receptors (TLRs), epithelial cells begin to synthesize various biologically active molecules. The pathophysiology of the COVID 19 is primarily attributed to the hyperactivation of host's immune system due to direct damage to the cells, with consequent release of proinflammatory substances, but also due to the activation of the innate immune response through the activation of alveolar macrophages and dendrite cells (DC). A strong proinflammatory reaction causes damage to alveolar epithelial cells and vascular endothelium. Respiratory epithelial cells, alveolar macrophages and DC are likely to be the most important cells involved in the innate immune response to the virus, since prolonged and excessive SARS-CoV-2-induced activation of these cells leads to the secretion of cytokines and chemokines that massively attract leukocytes and monocytes to the lungs and cause lung damage.

scholarly journals Toll-Like Receptor 2 Mediates Alveolar Macrophage Response to Pneumocystis murina

2006 ◽  
Vol 74 (3) ◽  
pp. 1857-1864 ◽  
Author(s):  
Chen Zhang ◽  
Shao-Hung Wang ◽  
Mark E. Lasbury ◽  
Dennis Tschang ◽  
Chung-Ping Liao ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Alveolar Macrophages ◽  
Nuclear Translocation ◽  
Innate Immune ◽  
Hek293 Cells ◽  
Mrna Levels ◽  
Toll Like Receptor ◽  
Tnf Α ◽  
Toll Like Receptor 2

ABSTRACT The innate immune response to Pneumocystis infection is not well understood. In this study, normal C57BL/6 mouse alveolar macrophages were found to respond to Pneumocystis murina organisms through Toll-like receptor 2 (TLR2), leading to the nuclear translocation of NF-κB and the production of proinflammatory cytokine tumor necrosis factor alpha (TNF-α) and chemokine macrophage inflammatory protein 2 (MIP-2). P. murina stimulation of normal alveolar macrophages from C57BL/6 mice resulted in increased TLR2 transcription but not increased TLR4 transcription. In gain-of-function studies with HEK293 cells expressing TLR2 or TLR4, only TLR2 was found to stimulate an NF-κB response to P. murina. TNF-α and MIP-2 production in response to P. murina by mouse alveolar macrophages was inhibited by a monoclonal antibody that specifically blocked the ligand-binding ability of TLR2. Alveolar macrophages from TLR2 knockout (TLR2−/−) mice showed little increase in TNF-α and MIP-2 mRNA levels upon P. murina stimulation. An in vivo study showed that TLR2−/− mice challenged with P. murina had reduced cytokine responses. These results indicate that TLR2 plays a major role in the innate immune response to P. murina.

scholarly journals Role of Dendritic Cells and Alveolar Macrophages in Regulating Early Host Defense against Pulmonary Infection with Cryptococcus neoformans

2009 ◽  
Vol 77 (9) ◽  
pp. 3749-3758 ◽  
Author(s):  
John J. Osterholzer ◽  
Jami E. Milam ◽  
Gwo-Hsiao Chen ◽  
Galen B. Toews ◽  
Gary B. Huffnagle ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Cryptococcus Neoformans ◽  
Innate Immune Response ◽  
Host Defense ◽  
Alveolar Macrophages ◽  
Pulmonary Infection ◽  
Innate Immune ◽  
Cellular Mechanisms

ABSTRACT Successful pulmonary clearance of the encapsulated yeast Cryptococcus neoformans requires a T1 adaptive immune response. This response takes up to 3 weeks to fully develop. The role of the initial, innate immune response against the organism is uncertain. In this study, an established model of diphtheria toxin-mediated depletion of resident pulmonary dendritic cells (DC) and alveolar macrophages (AM) was used to assess the contribution of these cells to the initial host response against cryptococcal infection. The results demonstrate that depletion of DC and AM one day prior to infection results in rapid clinical deterioration and death of mice within 6 days postinfection; this effect was not observed in infected groups of control mice not depleted of DC and AM. Depletion did not alter the microbial burden or total leukocyte recruitment in the lung. Mortality (in mice depleted of DC and AM) was associated with increased neutrophil and B-cell accumulation accompanied by histopathologic evidence of suppurative neutrophilic bronchopneumonia, cyst formation, and alveolar damage. Collectively, these data define an important role for DC and AM in regulating the initial innate immune response following pulmonary infection with C. neoformans. These findings provide important insight into the cellular mechanisms which coordinate early host defense against an invasive fungal pathogen in the lung.

scholarly journals Expression of Cathelicidin LL-37 during Mycobacterium tuberculosis Infection in Human Alveolar Macrophages, Monocytes, Neutrophils, and Epithelial Cells

2007 ◽  
Vol 76 (3) ◽  
pp. 935-941 ◽  
Author(s):  
Bruno Rivas-Santiago ◽  
Rogelio Hernandez-Pando ◽  
Claudia Carranza ◽  
Esmeralda Juarez ◽  
Juan Leon Contreras ◽  
...  
Keyword(s):  
Immune Response ◽  
Mycobacterium Tuberculosis ◽  
Epithelial Cells ◽  
Innate Immune Response ◽  
Alveolar Macrophages ◽  
Mycobacterial Infection ◽  
Innate Immune ◽  
Tuberculosis Infection ◽  
Mycobacterium Tuberculosis Infection ◽  
Peptide Expression

ABSTRACT The innate immune response in human tuberculosis is not completely understood. To improve our knowledge regarding the role of cathelicidin hCAP-18/LL37 in the innate immune response to tuberculosis infection, we used immunohistochemistry, immunoelectron microscopy, and gene expression to study the induction and production of the antimicrobial peptide in A549 epithelial cells, alveolar macrophages (AM), neutrophils, and monocyte-derived macrophages (MDM) after infection with Mycobacterium tuberculosis. We demonstrated that mycobacterial infection induced the expression and production of LL-37 in all cells studied, with AM being the most efficient. We did not detect peptide expression in tuberculous granulomas, suggesting that LL-37 participates only during early infection. Through the study of Toll-like receptors (TLR) in MDM, we showed that LL-37 can be induced by stimulation through TLR-2, TLR-4, and TLR-9. This last TLR was strongly stimulated by M. tuberculosis DNA. We concluded that LL-37 may have an important role in the innate immune response against M. tuberculosis.

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