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Example text
These infectious processes lead rapidly to ulceration (or even necrosis in the case of contamination by anaerobiosis) of the lower layers of the bronchial wall. The submucosal glands can be damaged by this process wherever they are situated. Edema and diffuse or focused leukocyte infiltration occur on the supporting tissue in areas of abscess where the base is covered with a leukofibrinous membrane and necrotic debris. Proliferative Processes The epithelium appears thickened and multilayered. This phenomenon is linked to the multiplication of all, or more often a variety of, constitutive cells: hyperplasia of the mucous cells and Clara cells under the effect of gases (NO2, O3) and multiplication of intermediary and basal cells due to the action of carcinogens.
Conclusion 86 References 87 5. Role of Neural Mechanisms in Airway Defense Peter J. Barnes 93 I. Introduction 93 II. Afferent Nerves 95 III. Cholinergic Nerves 100 IV. Neurogenic Inflammation 102 References 111 Page xiii 6. Role of Peptidases in Airway Defense Mechanisms Giovanni Piedimonte and Jay A. Nadel 123 I. Peptide-Containing Nerves in the Airways: NANC System 123 II. Modulation by Peptide-Degrading Enzymes: NEP and ACE 124 III. NEP and ACE in the Airways: Physiological Role 129 IV. Downregulation of NEP and ACE in the Airways: Possible Role in the Pathophysiology of Airway Inflammation 139 V.
Introduction 381 II. Nasopharyngeal Region 383 III. Large and Middle Airway Region 386 IV. Distal Airway and Alveolar Region 391 V. Cellular Level 402 VI. Conclusion 406 References 407 Page xvi Part IV: INFECTIOUS AGENTS AND THE AIRWAY 16. Changes in Airways Structure and Function After Viral Infection David B. Jacoby 415 I. Introduction 415 II. Acute Effects of Viral Infections 416 III. Chronic Effects of Viral Infections 427 IV. Summary 430 References 430 17. Bacterial Infection and Airways Epithelium Philippe Roussel, Geneviève Lamblin, and Reuben Ramphal 437 I.