P1-11 Nitric oxide and CD4+25+ Regulatory T cell production from iNOS knockout mice and their F1 mice treated with LPS

Mice deficient in inducible nitric oxide synthase (iNOS; C57Bl/6Ai-[KO] NOS2 N5) or wild-type C57Bl/6 mice were exposed to 1 part/million of ozone 8 h/night or to filtered air for three consecutive nights. Endpoints measured included lavagable total protein, macrophage inflammatory protein (MIP)-2, matrix metalloproteinase (MMP)-9, cell content, and tyrosine nitration of whole lung proteins. Ozone exposure caused acute edema and an inflammatory response in the lungs of wild-type mice, as indicated by significant increases in lavage protein content, MIP-2 and MMP-9 content, and polymorphonuclear leukocytes. The iNOS knockout mice showed significantly greater levels of lung injury by all of these criteria than did the wild-type mice. We conclude that iNOS knockout mice are more susceptible to acute lung damage induced by exposure to ozone than are wild-type C57Bl/6 mice and that protein nitration is associated with the degree of inflammation and not dependent on iNOS-derived nitric oxide.

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Nitric Oxide Mediates T Cell Cytokine Production and Signal Transduction in Histidine Decarboxylase Knockout Mice

The Journal of Immunology ◽

10.4049/jimmunol.179.10.6613 ◽

2007 ◽

Vol 179 (10) ◽

pp. 6613-6619 ◽

Cited By ~ 18

Author(s):

Agnes Koncz ◽

Maria Pasztoi ◽

Mercedesz Mazan ◽

Ferenc Fazakas ◽

Edit Buzas ◽

...

Keyword(s):

Nitric Oxide ◽

Signal Transduction ◽

T Cell ◽

Knockout Mice ◽

Cytokine Production ◽

Histidine Decarboxylase ◽

Cell Cytokine Production

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IL-33 and IgE stimulate mast cell production of IL-2 and regulatory T cell expansion in allergic dermatitis

Clinical & Experimental Allergy ◽

10.1111/cea.13027 ◽

2017 ◽

Vol 47 (11) ◽

pp. 1409-1416 ◽

Cited By ~ 13

Author(s):

P. Salamon ◽

I. Shefler ◽

I. Moshkovits ◽

A. Munitz ◽

D. Horwitz Klotzman ◽

...

Keyword(s):

Mast Cell ◽

T Cell ◽

Regulatory T Cell ◽

Cell Expansion ◽

Cell Production ◽

Allergic Dermatitis ◽

T Cell Expansion

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Investigation of Role of Nitric Oxide in Protection from Bordetella pertussis Respiratory Challenge

Infection and Immunity ◽

10.1128/iai.70.2.679-684.2002 ◽

2002 ◽

Vol 70 (2) ◽

pp. 679-684 ◽

Cited By ~ 24

Author(s):

C. Canthaboo ◽

D. Xing ◽

X. Q. Wei ◽

M. J. Corbel

Keyword(s):

Nitric Oxide ◽

Bordetella Pertussis ◽

Knockout Mice ◽

No Production ◽

Wild Type ◽

Respiratory Challenge ◽

Inos Knockout Mice ◽

Oxide Synthase

ABSTRACT The mechanism whereby whole-cell pertussis vaccines (WCV) confer protection against Bordetella pertussis is still not fully understood. We have previously reported that macrophage activation produced by vaccination with WCV is associated with induction of NO synthesis by macrophages in response to in vitro stimulation with B. pertussis antigens. To determine whether NO production is an effector of protection or simply a marker of activation, the susceptibility of inducible nitric oxide synthase (type II, iNOS) knockout mice to infection with B. pertussis was examined. We showed that iNOS knockout mice were more susceptible to B. pertussis respiratory challenge than wild-type mice. iNOS-deficient mice also developed a less effective protective response than wild-type mice after the same immunization with WCV. This suggests that NO plays an important role in effecting protection against B. pertussis challenge.

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