Occupational asthma and interleukin‐8

Lezcano-Meza, D; Teran, Luis M.

doi:10.1046/j.1365-2222.1999.00723.x

Cited by 9 publications

(4 citation statements)

References 24 publications

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“…Produced primarily by macrophages, IL-8 is one of the most important mediators in the recruitment of neutrophils to the respiratory tract (88). Neutrophils appear to be important inflammatory leukocytes in airway secretions of patients with acute severe asthma (89).…”

Section: Influence On Cytokine Expressionmentioning

confidence: 99%

Diesel exhaust and asthma: hypotheses and molecular mechanisms of action.

Pandya

Solomon

Kinner

et al. 2002

Environ Health Perspect

206

126

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Several components of air pollution have been linked to asthma. In addition to the well-studied critera air pollutants, such as nitrogen dioxide, sulfur dioxide, and ozone, diesel exhaust and diesel exhaust particles (DEPs) also appear to play a role in respiratory and allergic diseases. Diesel exhaust is composed of vapors, gases, and fine particles emitted by diesel-fueled compressionignition engines. DEPs can act as nonspecific airway irritants at relatively high levels. At lower levels, DEPs promote release of specific cytokines, chemokines, immunoglobulins, and oxidants in the upper and lower airway. Release of these mediators of the allergic and inflammatory response initiates a cascade that can culminate in airway inflammation, mucus secretion, serum leakage into the airways, and bronchial smooth muscle contraction. DEPs also may promote expression of the T H 2 immunologic response phenotype that has been associated with asthma and allergic disease. DEPs appear to have greater immunologic effects in the presence of environmental allergens than they do alone. This immunologic evidence may help explain the epidemiologic studies indicating that children living along major trucking thoroughfares are at increased risk for asthmatic and allergic symptoms and are more likely to have objective evidence of respiratory dysfunction.

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Section: Influence On Cytokine Expressionmentioning

confidence: 99%

Diesel exhaust and asthma: hypotheses and molecular mechanisms of action.

Pandya

Solomon

Kinner

et al. 2002

Environ Health Perspect

206

126

View full text Add to dashboard Cite

show abstract

“…IL-8, a member of CXC chemokine family mainly produced by macrophages, is one of the key mediators in attracting neutrophils to the airways (Lezcano-Meza et al, 1999).…”

Section: Modulation Of the Pulmonary Immune Responsesmentioning

confidence: 99%

Effect of diesel exhaust particles on allergic reactions and airway responsiveness in ovalbumin-sensitized brown Norway rats

Dong¹

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Diesel exhaust particles (DEP) are the major constituent of ambient particulate matter in urban environments and occupational settings. Exposure to DEP in combination with an allergen has been demonstrated to enhance allergen-related airway inflammation, immunoglobulin (Ig) E production, and airway responsiveness (AR) in human and in animal models. However, the mechanisms behind these effects of DEP are not yet fully understood. In this study, we compared the effects of short-term DEP exposure on ovalbumin (OVA)-mediated airway responses under two exposure protocols using an OVA-allergic rat model. Male Brown Norway rats were sensitized to aerosolized OVA (40.5 ± 6.3 mg/m 3) on days 1, 8, and 15, and challenged with OVA on day 29. The rats were exposed to DEP (20 mg/m 3) for 4 h/day for 5 consecutive days either before sensitization (protocol A) or before OVA challenge on days 24-28 (protocol B). Control animals received filtered air and aerosolized saline instead of DEP and OVA, respectively. The results showed that DEP exposure 1) elicited an adjuvant effect on OVA-specific IgE and IgG production in serum under both protocols; 2) significantly reduced OVA-induced airway inflammation and lung injury in protocol A, but increased these markers in protocol B; 3) markedly lowered OVA-induced production of nitric oxide, reactive oxygen species, and interleukin (IL)-10 and IL-12 by alveolar macrophages (AM) in protocol A, but increased these parameters in protocol B; 4) significantly lowered the numbers of T cells and their CD4 + and CD8 + subsets in lungdraining lymph nodes in protocol A, but increased these cell counts in protocol B; 5) reduced intracellular glutathione in AM and lymphocytes in both protocols; and 6) enhanced AR of the OVA-sensitized rats to methacholine challenge in protocol B. These results suggest that the effects of DEP on the immune system, including aggravation or exacerbation of asthma, may be greatly influenced by allergic immune status and time of antigen exposure. vi

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“… 1 Elevated CXCL8 levels are typical in airway diseases such as chronic obstructive pulmonary disease, cystic fibrosis, and severe asthma, and are believed to be an important factor in the pathogenesis of such disorders. 2 – 4 In addition, CXCL8 also has mitogenic, motogenic, and angiogenic properties and may contribute to cancer development. 5 Thus, elucidating the mechanisms of CXCL8 regulation is of considerable therapeutic interest.…”

Section: Introductionmentioning

confidence: 99%

Differential NF-κB and MAPK activation underlies fluoride- and TPA-mediated CXCL8 (IL-8) induction in lung epithelial cells

Refsnes¹,

Skuland²,

Låg³

et al. 2014

JIR

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Different toxic agents have a varying potential to induce the production of the proinflammatory chemokine, CXCL8 (interleukin [IL]-8), in lung cells. A critical question is which mechanisms determine the magnitude and persistence of the CXCL8 responses to different stimuli. To approach this, we compared the potential of the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), and sodium fluoride (NaF) to induce CXCL8 responses in A549 cells, with emphasis on the importance of nuclear factor kappa B (NF-κB)- and mitogen-activated protein kinase (MAPK) signaling. Notably, TPA induced a greater release of CXCL8 than did NaF. Furthermore, TPA induced a strong, rapid, but transient upregulation of CXCL8 messenger (m)RNA, whereas NaF induced a weaker, more delayed, but persistent upregulation. With respect to signaling, TPA led to an early, strong, and relatively transient extracellular signal-regulated kinase (ERK)1/2 phosphorylation, and a less marked and even more transient phosphorylation of c-jun-N-terminal kinases (JNK1/2) and p38. In contrast, NaF elicited a lower, but relatively sustained increase in phosphorylation of ERK1/2, and a marked phosphorylation of p38 and JNK1/2, with the JNK1/2 response as most transient. Only ERK1/2 inhibition affected the TPA response, whereas inhibition of all the three MAPK cascades reduced NaF-induced CXCL8 release. TPA also induced an early, marked phosphorylation/translocation of p65 (NF-κB), whereas NaF induced slower, less pronounced effects on p65. The CXCL8 responses by TPA and NaF were reduced by p65-siRNA. In conclusion, all MAPK cascades were involved in NaF-induced CXCL8 release, whereas only ERK1/2 activation was involved in response to TPA. Furthermore, NF-κB activation appeared to be indispensable for CXCL8 induction. The early response, magnitude, and persistency of MAPK and NF-κB signaling seemed to be critical determinants for the potential to induce CXCL8. These findings underscore that a strong, rapid, and relatively transient activation of ERK1/2 in combination with NF-kB may be sufficient for a strong induction of CXCL8, which may exceed the effects of a more moderate ERK1/2 activation in combination with activation of p38, JNK1/2, and NF-κB.

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Occupational asthma and interleukin‐8

Cited by 9 publications

References 24 publications

Diesel exhaust and asthma: hypotheses and molecular mechanisms of action.

Diesel exhaust and asthma: hypotheses and molecular mechanisms of action.

Effect of diesel exhaust particles on allergic reactions and airway responsiveness in ovalbumin-sensitized brown Norway rats

Differential NF-κB and MAPK activation underlies fluoride- and TPA-mediated CXCL8 (IL-8) induction in lung epithelial cells

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Occupational asthma and interleukin‐8

Cited by 9 publications

References 24 publications

Diesel exhaust and asthma: hypotheses and molecular mechanisms of action.

Diesel exhaust and asthma: hypotheses and molecular mechanisms of action.

Effect of diesel exhaust particles on allergic reactions and airway responsiveness in ovalbumin-sensitized brown Norway rats

Differential NF-&kappa;B and MAPK activation underlies fluoride- and TPA-mediated CXCL8 (IL-8) induction in lung epithelial cells

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Differential NF-κB and MAPK activation underlies fluoride- and TPA-mediated CXCL8 (IL-8) induction in lung epithelial cells