Induction of Interleukin 8 (IL‐8) Production by <i>Pseudomonas</i> Nitrite Reductase in Human Alveolar Macrophages and Epithelial Cells

Sar, Borann; Oishi, Kazunori; Matsushima, Kouji; Nagatake, Tsuyoshi

doi:10.1111/j.1348-0421.1999.tb02424.x

Cited by 11 publications

(11 citation statements)

References 27 publications

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“…Taken together, these results clearly demonstrate that the NTHi-induced release of IL-8 is mediated through TLR2, but is not secondary to an increase in the production of TNF-a. The TNF-a-independent production of IL-8 was reported in both human macrophages and A549 cells treated with Pseudomonas nitrite reductase (27), and in primary human monocytes treated with Neisseria gonorrhoeae (28).…”

Section: The Nthi Lysate-induced Expression Of Muc1 Is Tnf-a-dependentmentioning

confidence: 99%

Antiinflammatory Role of MUC1 Mucin during Infection with NontypeableHaemophilus influenzae

Kyo

Kato

Park

et al. 2012

Am J Respir Cell Mol Biol

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MUC1 (or Muc1 in nonhuman species) is a membrane-tethered mucin expressed on the apical surface of mucosal epithelia (including those of the airways) that suppresses Toll-like receptor (TLR) signaling. We sought to determine whether the anti-inflammatory effect of MUC1 is operative during infection with nontypeable Haemophilus influenzae (NTHi), and if so, which TLR pathway was affected. Our results showed that: (1) a lysate of NTHi increased the early release of IL-8 and later production of MUC1 protein by A549 cells in dose-dependent and time-dependent manners, compared with vehicle control; (2) both effects were attenuated after transfection of the cells with a TLR2-targeting small interfering (si) RNA, compared with a control siRNA; (3) the NTHi-induced release of IL-8 was suppressed by an overexpression of MUC1, and was enhanced by the knockdown of MUC1; (4) the TNF-a released after treatment with NTHi was sufficient to up-regulate MUC1, which was completely inhibited by pretreatment with a soluble TNF-a receptor; and (5) primary murine tracheal surface epithelial (MTSE) cells from Muc1 knockout mice exhibited an increased in vitro production of NTHi-stimulated keratinocyte chemoattractant compared with MTSE cells from Muc1-expressing animals. These results suggest a hypothetical feedback loop model whereby NTHi activates TLRs (mainly TLR2) in airway epithelial cells, leading to the increased production of TNF-a and IL-8, which subsequently up-regulate the expression of MUC1, resulting in suppressed TLR signaling and decreased production of IL-8. This report is the first, to the best of our knowledge, demonstrating that the inflammatory response in airway epithelial cells during infection with NTHi is controlled by MUC1 mucin, mainly through the suppression of TLR2 signaling.

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Section: The Nthi Lysate-induced Expression Of Muc1 Is Tnf-a-dependentmentioning

confidence: 99%

Antiinflammatory Role of MUC1 Mucin during Infection with NontypeableHaemophilus influenzae

Kyo

Kato

Park

et al. 2012

Am J Respir Cell Mol Biol

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“…Henderson et al (26) have suggested that bacterial factors (i.e., modulins) beyond LPS play a role in the induction of cytokine synthesis by host cells. For example, cell surface adhesins (pilin and flagellin), secreted products (autoinducer and pyocyanin), and periplasmic components (nitrite reductase) of P. aeruginosa stimulated IL-8 production from a variety of human respiratory epithelial cells (8,10,54,63). P. aeruginosa LPS, however, minimally stimulated IL-8 production from the respiratory epithelial cells (10,54).…”

Section: Discussionmentioning

confidence: 99%

“…Further, LBP alone cannot mediate cellular responses to LPS independent of CD14 (71). Levels of respiratory epithelial cytokine stimulation by LPS/LOS vary greatly; this variation may depend on the bacterial source and structure of the LPS/LOS (10,18,51,54,59,63,64,70). The actual signaling pathway for H. influenzae LOS-mediated stimulation of respiratory epithelial cytokine production remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

“…Several respiratory pathogens such as Pseudomonas aeruginosa, Burkholderia cepacia, Streptococcus pneumoniae, and Bordetella pertussis produce a variety of molecules that interact with epithelial cells and cause a secretion of proinflammatory cytokines (10,19,25,26,29,39,54,58,63,74,76). These interactions involve bacterial cell-associated and extracellular products that include cell wall fragments, outer membrane proteins, autoinducers, pili and flagella, and secreted molecules.…”

mentioning

confidence: 99%

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Induction of Proinflammatory Cytokines from Human Respiratory Epithelial Cells after Stimulation by NontypeableHaemophilus influenzae

et al. 2000

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Nontypeable Haemophilus influenzae (NTHi) causes repeated respiratory infections in patients with chronic lung diseases. These infections are characterized by a brisk inflammatory response which results in the accumulation of polymorphonucleated cells in the lungs and is dependent on the expression and secretion of proinflammatory cytokines. We hypothesize that multiple NTHi molecules, including lipooligosaccharide (LOS), mediate cellular interactions with respiratory epithelial cells, leading to the production of proinflammatory cytokines. To address this hypothesis, we exposed 9HTEo؊ human tracheal epithelial cells to NTHi and compared the resulting profiles of cytokine gene expression and secretion using multiprobe RNase protection assays and enzyme-linked immunosorbent assays (ELISA), respectively. Dose-response experiments demonstrated a maximum stimulation of most cytokines tested, using a ratio of 100 NTHi bacterial cells to 1 9HTEo؊ tracheal epithelial cell. Compared with purified LOS, NTHi bacterial cells stimulated 3.6-and 4.5-fold increases in epithelial cell expression of interleukin-8 (IL-8) and IL-6 genes, respectively. Similar results were seen with epithelial cell macrophage chemotactic protein 1, IL-1␣, IL-1␤, and tumor necrosis factor alpha expression. Polymyxin B completely inhibited LOS stimulation but only partially reduced NTHi whole cell stimulation. Taken together, these results suggest that multiple bacterial molecules including LOS contribute to the NTHi stimulation of respiratory epithelial cell cytokine production. Moreover, no correlation was seen between NTHi adherence to epithelial cells mediated by hemagglutinating pili, Hia, HMW1, HMW2, and Hap and epithelial cytokine secretion. These data suggest that bacterial molecules beyond previously described NTHi cell surface adhesins and LOS play a role in the induction of proinflammatory cytokines from respiratory epithelial cells.

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“…ELR ϩ CXC chemokines have recently been shown to be induced in gram-negative bacterial pneumonia models. In vitro studies have shown that many virulent factors of P. aeruginosa induce robust IL-8 production from isolated neutrophils, alveolar macrophages, as well as respiratory bronchial and alveolar epithelia (4,8,9,28,31,33,37). Furthermore, a recent in vivo study of P. aeruginosa bronchopulmonary infection in CF mice demonstrated that retention of bacteria in the airways induced an excessive inflammatory response in CF mice above that of wild-type mice challenged with comparable bacterial inoculum (18).…”

mentioning

confidence: 99%

CXC Chemokine Receptor CXCR2 Is Essential for Protective Innate Host Response in MurinePseudomonas aeruginosaPneumonia

et al. 2000

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Induction of Interleukin 8 (IL‐8) Production by Pseudomonas Nitrite Reductase in Human Alveolar Macrophages and Epithelial Cells

Abstract: Abstract:Interleukin-8

Cited by 11 publications

References 27 publications

Antiinflammatory Role of MUC1 Mucin during Infection with NontypeableHaemophilus influenzae

Antiinflammatory Role of MUC1 Mucin during Infection with NontypeableHaemophilus influenzae

Induction of Proinflammatory Cytokines from Human Respiratory Epithelial Cells after Stimulation by NontypeableHaemophilus influenzae

CXC Chemokine Receptor CXCR2 Is Essential for Protective Innate Host Response in MurinePseudomonas aeruginosaPneumonia

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