Late Phase Reactions Induce Localized Inflammatory Reactions

As a type I hypersensitive reaction begins to subside, mediators released during the course of the reaction often induce localized inflammation called the late-phase reaction. Distinct from the late response seen in asthma, the late-phase reaction begins to develop 4-6 h after the initial type I reaction and persists for 1-2 days. The reaction is characterized by infiltration of neutrophils, eosinophils, macrophages, lymphocytes, and basophils. The localized late-phase response also may be mediated partly by cytokines released from mast cells.

EARLY RESPONSE

LATE RESPONSE

Mucous glands

Inflammatory cells (eosinophils; neutrophils)

LATE RESPONSE

Mucous glands

EARLY RESPONSE

Early And Late Asthmatic Reaction

Inflammatory cells (eosinophils; neutrophils)

Thickened basement membrane

Thickened basement membrane

EARLY RESPONSE (minutes)

LATE RESPONSE (hours)

Histamine

PGD LTC4

Vasodilation Bronchoconstriction Mucus secretion

Increased endothelial cell adhesion Leukocyte migration Leukocyte activation

The early and late inflammatory responses in asthma. sented at the top. The effects of various mediators on an airway, repre-The immune cells involved in the early and late responses are repre- sented in cross section, are illustrated in the center.

FIGURE 16-8

Both TNF-a and IL-1 increase the expression of cell-adhesion molecules on venular endothelial cells, thus facilitating the buildup of neutrophils, eosinophils, and monocytes that characterizes the late-phase response.

Eosinophils play a principal role in the late-phase reaction, accounting for some 30% of the cells that accumulate. Eosinophil chemotactic factor, released by mast cells during the initial reaction, attracts large numbers of eosinophils to the affected site. Various cytokines released at the site, including IL-3, IL-5, and GM-CSF, contribute to the growth and differentiation of the eosinophils. Eosinophils express Fc receptors for IgG and IgE isotypes and bind directly to antibody-coated allergen. Much as in mast-cell degranulation, binding of antibody-coated antigen activates eosino-phils, leading to their degranulation and release of inflammatory mediators, including leukotrienes, major basic protein, platelet-activation factor, eosinophil cationic protein (ECP), and eosinophil-derived neurotoxin. The release of these eosinophil-derived mediators may play a protective role in parasitic infections. However, in response to allergens, these mediators contribute to extensive tissue damage in the late-phase reaction. The influx of eosinophils in the late-phase response has been shown to contribute to the chronic inflammation of the bronchial mucosa that characterizes persistent asthma.

Neutrophils are another major participant in late-phase reactions, accounting for another 30% of the inflammatory cells. Neutrophils are attracted to the area of a type I reaction by neutrophil chemotactic factor, released from degranulat-ing mast cells. In addition, a variety of cytokines released at the site, including IL-8, have been shown to activate neutrophils, resulting in release of their granule contents, including lytic enzymes, platelet-activating factor, and leukotrienes.

Coping with Asthma

Coping with Asthma

If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.

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Responses

  • jari
    How to induce "localized inflammation"?
    5 months ago

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