Induction of CXCL5 During Inflammation in the Rodent Lung Involves Activation of Alveolar Epithelium

Jeyaseelan, Samithamby; Manzer, Rizwan; Young, Shamar; Yamamoto, Masahiro; Akira, Shizuo; Mason, Robert J.; Worthen, G. Scott

doi:10.1165/rcmb.2005-0063oc

Cited by 137 publications

(158 citation statements)

References 37 publications

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“…5, E and J). In this context, we have demonstrated that LIX is predominantly produced by resident cells, i.e., alveolar type II cells after LPS challenge (25,26).…”

Section: Discussionmentioning

confidence: 90%

“…Proposed scheme for TRIF-dependent signaling cascade leading to neutrophil influx in the lungs (in vivo) in response to E. coli and E. coli LPS. E. coli activates TLR4 and other receptor(s) to induce a cascade that involves TRIF, whereas E. coli LPS activates TLR4-mediated TRIF-dependent signaling (25). This cascade is important for the LIX production and subsequent neutrophil accumulation in the lungs (in vivo).…”

Section: Discussionmentioning

confidence: 99%

“…The induction of lung inflammation in a murine model by LPS aerosolization has been described in our previous studies (25)(26)(27)(28). Briefly, mice were exposed to 0.3 mg of LPS/ml in 0.9% saline by aerosolization for 20 min under a laminar flow hood by using a flow rate of 2 L/min.…”

Section: Mouse Lps Challenge Protocolmentioning

confidence: 99%

“…A midventral incision was used to open the thoracic cavity, and the trachea was isolated and cannulated with a 20-gauge catheter. BALF was obtained from the whole lung to collect cells in the airspace and to obtain proteins for cytokine and chemokine detection, as described previously (25)(26)(27)(28). A total of 3.0 ml of BALF was retrieved from each mouse, and 0.5 ml of BALF was centrifuged and placed on glass cytospin slides, which were then stained by modified Wright-Giemsa staining (Diff-Quick; Fisher Scientific) to determine leukocyte subtypes based on their cellular and nuclear morphology.…”

Section: Bronchoalveolar Lavage Fluid (Balf) Collectionmentioning

confidence: 99%

“…Cytokine and chemokine levels were assessed in BALF or culture supernatants of bone marrow-derived macrophage (BMM) cultures using a cytokine-or chemokine-specific sandwich ELISA, as described in our earlier publications (25)(26)(27)(28). The minimum detection limit is 2 pg/ml cytokine or chemokine protein.…”

Section: Cytokine and Chemokine Determination In Balfmentioning

confidence: 99%

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Toll/IL-1 Receptor Domain-Containing Adaptor Inducing IFN-β (TRIF)-Mediated Signaling Contributes to Innate Immune Responses in the Lung during Escherichia coli Pneumonia

Jeyaseelan

Young

Fessler

et al. 2007

The Journal of Immunology

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Bacterial pneumonia remains a serious disease and is associated with neutrophil recruitment. Innate immunity is pivotal for the elimination of bacteria, and TLRs are essential in this process. Toll/IL-1R domain-containing adaptor inducing IFN-β (TRIF) is an adaptor for TLR3 and TLR4, and is associated with the MyD88-independent cascade. However, the importance of TRIF in immune responses against pulmonary bacterial pathogens is not well understood. We investigated the involvement of TRIF in a murine model of Escherichia coli pneumonia. TRIF−/− mice infected with E. coli display attenuated neutrophil migration; NF-κB activation; and TNF-α, IL-6, and LPS-induced C-X-C chemokine production in the lungs. In addition, E. coli-induced phosphorylation of JNK, ERK, and p38 MAPK was detected in bone marrow-derived macrophages (BMMs) of TRIF+/+ mice, but attenuated in BMMs of TRIF−/− mice. Furthermore, E. coli-induced TNF-α and IL-6 production was attenuated in BMMs of TRIF−/− mice. E. coli LPS-induced late MAPK activation, and TNF-α and IL-6 production were abolished in BMMs of TRIF−/− mice. Moreover, TRIF is not required for LPS-induced neutrophil influx, and keratinocyte cell-derived chemokine, MIP-2, and LPS-induced C-X-C chemokine production in the lungs. Using TLR3−/− mice, we ruled out the role of TLR3-mediated TRIF-dependent neutrophil influx during E. coli pneumonia. A TLR4-blocking Ab inhibited E. coli-induced TNF-α and IL-6 in BMMs of both TRIF−/− and TRIF+/+ mice, suggesting that TRIF-mediated signaling involves TLR4. We also found that TRIF is critical to control E. coli burden in the lungs and E. coli dissemination. Thus, rapid activation of TRIF-dependent TLR4-mediated signaling cascade serves to augment pulmonary host defense against a Gram-negative pathogen.

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“…5, E and J). In this context, we have demonstrated that LIX is predominantly produced by resident cells, i.e., alveolar type II cells after LPS challenge (25,26).…”

Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Mouse Lps Challenge Protocolmentioning

confidence: 99%

Section: Bronchoalveolar Lavage Fluid (Balf) Collectionmentioning

confidence: 99%

Section: Cytokine and Chemokine Determination In Balfmentioning

confidence: 99%

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Toll/IL-1 Receptor Domain-Containing Adaptor Inducing IFN-β (TRIF)-Mediated Signaling Contributes to Innate Immune Responses in the Lung during Escherichia coli Pneumonia

Jeyaseelan

Young

Fessler

et al. 2007

The Journal of Immunology

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Type I IFN signaling triggers immunopathology in tuberculosis‐susceptible mice by modulating lung phagocyte dynamics

et al. 2014

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General interest in the biological functions of IFN type I in Mycobacterium tuberculosis (Mtb) infection increased after the recent identification of a distinct IFN gene expression signature in tuberculosis (TB) patients. Here, we demonstrate that TB-susceptible mice lacking the receptor for IFN I (IFNAR1) were protected from death upon aerogenic infection with Mtb. Using this experimental model to mimic primary progressive pulmonary TB, we dissected the immune processes affected by IFN I. IFNAR1 signaling did not affect T-cell responses, but markedly altered migration of inflammatory monocytes and neutrophils to the lung. This process was orchestrated by IFNAR1 expressed on both immune and tissue-resident radioresistant cells. IFNAR1-driven TB susceptibility was initiated by augmented Mtb replication and in situ death events, along with CXCL5/CXCL1-driven accumulation of neutrophils in alveoli, followed by the discrete compartmentalization of Mtb in lung phagocytes. Early depletion of neutrophils rescued TB-susceptible mice to levels observed in mice lacking IFNAR1. We conclude that IFN I alters early innate events at the site of Mtb invasion leading to fatal immunopathology. These data furnish a mechanistic explanation for the detrimental role of IFN I in pulmonary TB and form a basis for understanding the complex roles of IFN I in chronic inflammation.

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Pulmonary response to surface‐coated nanotitanium dioxide particles includes induction of acute phase response genes, inflammatory cascades, and changes in microRNAs: A toxicogenomic study

Halappanavar

Jackson

Williams

et al. 2011

Environ and Mol Mutagen

152

137

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Titanium dioxide nanoparticles (nanoTiO2) are used in various applications including in paints. NanoTiO2 inhalation may induce pulmonary toxicity and systemic effects. However, the underlying molecular mechanisms are poorly understood. In this study, the effects of inhaled surface-coated nanoTiO2 on pulmonary global messenger RNA (mRNA) and microRNA (miRNA) expression in mouse were characterized to provide insight into the molecular response. Female C57BL/6BomTac mice were exposed for 1 hr daily to 42.4 ± 2.9 (SEM) mg surface-coated nanoTiO2/m3 for 11 consecutive days by inhalation and were sacrificed 5 days following the last exposure. Physicochemical properties of the particles were determined. Pulmonary response to nanoTiO2 was characterized using DNA microarrays and pathway-specific PCR arrays and related to data on pulmonary inflammation from bronchial lavages. NanoTiO2 exposure resulted in increased levels of mRNA for acute phase markers serum amyloid A-1 (Saa1) and serum amyloid A-3 (Saa3), several C-X-C and C-C motif chemokines, and cytokine tumor necrosis factor genes. Protein analysis of Saa1 and 3 showed selective upregulation of Saa3 in lung tissues. Sixteen miRNAs were induced by more than 1.2-fold (adjusted P-value < 0.05) following exposure. Real time polymerase chain reaction confirmed the upregulation of miR-1, miR-449a and revealed dramatic induction of miR-135b (60-fold). Thus, inhalation of surface-coated nanoTiO2 results in changes in the expression of genes associated with acute phase, inflammation and immune response 5 days post exposure with concomitant changes in several miRNAs. The role of these miRNAs in pulmonary response to inhaled particles is unknown and warrants further research. Environ. Mol. Mutagen., 2011. © 2011 Wiley-Liss, Inc.†

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Induction of CXCL5 During Inflammation in the Rodent Lung Involves Activation of Alveolar Epithelium

Cited by 137 publications

References 37 publications

Toll/IL-1 Receptor Domain-Containing Adaptor Inducing IFN-β (TRIF)-Mediated Signaling Contributes to Innate Immune Responses in the Lung during Escherichia coli Pneumonia

Toll/IL-1 Receptor Domain-Containing Adaptor Inducing IFN-β (TRIF)-Mediated Signaling Contributes to Innate Immune Responses in the Lung during Escherichia coli Pneumonia

Type I IFN signaling triggers immunopathology in tuberculosis‐susceptible mice by modulating lung phagocyte dynamics

Pulmonary response to surface‐coated nanotitanium dioxide particles includes induction of acute phase response genes, inflammatory cascades, and changes in microRNAs: A toxicogenomic study

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