The Concept of Neurogenic Inflammation in the Respiratory Tract

Neuropeptides such as substance P are implicated in inflammation mediated by sensory nerves (neurogenic inflammation), but the roles in disease of these peptides and the peptidases that degrade them are not understood. It is well established that inflammation is a prominent feature of several airway diseases, including viral infections, asthma, bronchitis, and cystic fibrosis. These diseases are characterized by cough, airway edema, and abnormal secretory and bronchoconstrictor responses, all of which can be elicited by substance P. The effects of substance P and other peptides that may be involved in inflammation are decreased by endogenous neutral endopeptidase (NEP; also called enkephalinase, EC 3.4.24.11), which is a peptidase that degrades substance P and other peptides. In the present study, we report that rats with histories of infections caused by common respiratory tract pathogens (parainfluenza virus type 1, rat corona-virus, and Mycoplasma pulmonis) not only have greater susceptibility to neurogenic inflammatory responses than do pathogen-free rats but also have a lower activity of NEP in the trachea. This reduction in NEP activity may cause the increased susceptibility to neurogenic inflammation by allowing higher concentrations of substance P to reach tachykinin receptors in the trachea. Thus decreased NEP activity may exacerbate some of the pathological responses in animals with respiratory tract infections.

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Mycoplasma pulmonis infections cause long-lasting potentiation of neurogenic inflammation in the respiratory tract of the rat.

Journal of Clinical Investigation ◽

10.1172/jci115082 ◽

1991 ◽

Vol 87 (3) ◽

pp. 787-799 ◽

Cited By ~ 38

Author(s):

D M McDonald ◽

T R Schoeb ◽

J R Lindsey

Keyword(s):

Respiratory Tract ◽

Neurogenic Inflammation ◽

Mycoplasma Pulmonis

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New Ultrastructural Observations on Injury and Regeneration of Cilia in Mammalian Conducting Airway Epithelium

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100099544 ◽

1981 ◽

Vol 39 ◽

pp. 624-625

Author(s):

J.L. Carson ◽

A.M. Collier

Keyword(s):

Respiratory Tract ◽

Airway Epithelium ◽

Defense Mechanisms ◽

Normal Growth ◽

Fetal Lung ◽

Secretory Cells ◽

Airway Epithelial ◽

Ciliated Cells ◽

Conducting Airway ◽

Conducting Airways

The ciliated cells lining the conducting airways of mammals are integral to the defense mechanisms of the respiratory tract, functioning in coordination with secretory cells in the removal of inhaled and cellular debris. The effects of various infectious and toxic agents on the structure and function of airway epithelial cell cilia have been studied in our laboratory, both of which have been shown to affect ciliary ultrastructure.These observations have led to questions about ciliary regeneration as well as the possible induction of ciliogenesis in response to cellular injury. Classical models of ciliogenesis in the conducting airway epithelium of the mammalian respiratory tract have been based primarily on observations of the developing fetal lung. These observations provide a plausible explanation for the embryological generation of ciliary beds lining the conducting airways but do little to account for subsequent differentiation of ciliated cells and ciliogenesis during normal growth and development.

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