Genes other than TLR4 are involved in the response to inhaled LPS

Lorenz, Eva; Jones, Michael P.; Wohlford‐Lenane, Christine L.; Meyer, Nicole C.; Frees, Kathy; Arbour, Nancy C.; Schwartz, David A.

doi:10.1152/ajplung.2001.281.5.l1106

Cited by 77 publications

(64 citation statements)

References 23 publications

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“…In addition, the LPS in the OVA exposures may have been responsible for increase of neutrophils present. All the mouse strains that had increased neutrophilia in our study have been found to respond to aerosolized LPS (29). Furthermore, the C3H/HeJ strain, which is unresponsive to LPS (29), did not have increased neutrophilia after OVA sensitization and challenge.…”

Section: Discussionmentioning

confidence: 53%

Allergen-induced airway disease is mouse strain dependent

Whitehead

Walker

Berman

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

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169

119

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We investigated the development of airway hyperreactivity (AHR) and inflammation in the lungs of nine genetically diverse inbred strains of mice [129/SvIm, A/J, BALB/cJ, BTBR+(T)/tf/tf, CAST/Ei, C3H/HeJ, C57BL/6J, DBA/2J, and FVB/NJ] after sensitization and challenge with ovalbumin (OVA). At 24, 48, and 72 h post-OVA exposure, the severity of AHR and eosinophilic inflammation of the mouse strains ranged from relatively unresponsive to responsive. The severity of the airway eosinophilia of some strains did not clearly correlate with the development of AHR. The temporal presence of T helper type 2 cytokines in lung lavage fluid also varied markedly among the strains. The levels of IL-4 and IL-13 were generally increased in the strains with the highest airway eosinophilia at 24 and 72 h postexposure, respectively; the levels of IL-5 were significantly increased in most of the strains with airway inflammation over the 72-h time period. The differences of physiological and biological responses among the inbred mouse strains after OVA sensitization and challenge support the hypothesis that genetic factors contribute, in part, to the development of allergen-induced airway disease.

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Section: Discussionmentioning

confidence: 53%

Allergen-induced airway disease is mouse strain dependent

Whitehead

Walker

Berman

et al. 2003

American Journal of Physiology-Lung Cellular and Molecular Phys

Self Cite

169

119

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“…In general, inhalation or nasal aspiration of endotoxin by mice induces similar host responses and changes (35,39), and these reflect human airway responsiveness (33).…”

Section: Discussionmentioning

confidence: 99%

MD-2–Dependent Pulmonary Immune Responses to Inhaled Lipooligosaccharides

Hađina¹,

Weiss²,

McCray³

et al. 2008

Am J Respir Cell Mol Biol

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Endotoxins represent one of the most potent classes of microbial immunoactive components that can cause pulmonary inflammation. The aim of this study was to compare the inflammatory potency of two types of Neisseria meningitidis endotoxins (lipooligosaccharides) in lungs: wild type (hexaacylated, LOS wt ) and mutant type (pentaacylated, LOS msbB ), and to determine the importance of MD-2 in endotoxin responses in lungs in vivo. Endotoxin-normoresponsive mice (BALB/c) were exposed to selected doses of penta-and hexaacylated lipooligosaccharides (LOS) by nasal aspiration. Cellular and cytokine/chemokine inflammatory responses in bronchoalveolar lavage were measured at 1-, 4-, 8-, 16-, 24-, and 48-hour time points. MD-2-null mice were exposed to one dose of hexaacylated LOS and inflammatory responses were measured after 4 and 24 hours. Inhalation of hexaacylated LOS resulted in strong inflammatory responses, while pentaacylated LOS was much less potent in inducing increases of neutrophils, TNF-a, macrophage inflammatory protein-1a, IL-6, granulocyte colony-stimulating factor, and IL-1b concentration in bronchoalveolar lavage. Similar kinetics of inflammatory responses in lungs were found in both types of endotoxin exposures. Inhalation of hexaacylated LOS in MD-2-null mice resulted in significantly lower numbers of neutrophils in bronchoalveolar lavage than in normoresponsive mice. Markedly lower inflammatory potency of pentaacylated LOS was observed compared with hexaacylated LOS. Hyporesponsiveness in MD-2-null mice after nasal aspiration of wild-type LOS indicate its essential role in airway responsiveness to endotoxin.

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“…The coupled role for TLR4 and induction of iNOS has been indicated in different organs, such as a TLR4-triggered iNOS expression and hyperpermeability in response to ozone exposure in the lungs (Jones et al 2001, Kleeberger et al 2001, and a correlated TLR4 expression with iNOS/NO actions in the myocardium during heart failure (Frantz et al 1999). Furthermore, among macrophages the LPS-induced iNOS response is significantly higher in those that express high numbers of TLR4 (Dil and Qureshi 2002).…”

Section: Alterations In Nnos By MD Cells As Part Of Compensatory Intementioning

confidence: 99%

Expression of nitric oxide synthase isoforms in the mouse kidney: cellular localization and influence by lipopolysaccharide and Toll-like receptor 4

et al. 2006

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We determined the cellular mRNA expression of all intrarenal nitric oxide (NO)-producing NO synthase (NOS) isoforms, endothelial NOS (eNOS) and neuronal NOS (nNOS) and inducible NOS (iNOS) in kidneys from wild type mice (WT) and immune deficient Toll-like receptor 4 (TLR4) mutant mice, during normal physiological conditions and during a shortterm (6-16 hours) endotoxic condition caused by systemically administered lipopolysaccaride (LPS). Investigations were performed by means of in situ hybridization and polymerase chain reaction amplification techniques. In WT, LPS altered the expression rate of all intrarenal NOS isoforms in a differentiated but NOS-isoform coupled expression pattern, with iNOS induction, and up-and down-regulation of the otherwise constitutively expressed NOS isoforms, e.g. eNOS and nNOS and an iNOS isotype. In TLR4 mutants, LPS caused none or a lowered iNOS induction, but altered the expression rate of the constitutive NOS isoforms. It is concluded that the intrarenal spatial relation of individual NOS-isoforms and their alteration in expression provide the basis for versatile NO-mediated renal actions that may include local interactions between NOS isoforms and their individual NO-target sites, and that the NOSisoform dependent events are regulated by TLR4 during endotoxic processes. These regulatory mechanisms are likely to participate in different pathophysiological conditions affecting NO-mediated renal functions.

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Genes other than TLR4 are involved in the response to inhaled LPS

Cited by 77 publications

References 23 publications

Allergen-induced airway disease is mouse strain dependent

Allergen-induced airway disease is mouse strain dependent

MD-2–Dependent Pulmonary Immune Responses to Inhaled Lipooligosaccharides

Expression of nitric oxide synthase isoforms in the mouse kidney: cellular localization and influence by lipopolysaccharide and Toll-like receptor 4

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