Polymorphonuclear leukocytes mast cells

Fiberoptic bronchoscopy with bronchoalveolar lavage (BAL) contributed significant insights into the pathogenesis of IPF and other ILDs but practical value is limited (2,147). Increases in polymorphonuclear leukocytes, mast cells, alveolar macrophages, and myriad cytokines are noted in BAL fluid from patients with IPF lymphocyte numbers are usually normal (147). However, BAL cell profiles in IPF do not predict prognosis or therapeutic responsiveness (147). We do not believe BAL cell counts have a role to stage or follow IPF. 

The first immune cells to recognize the foreign body and to be activated are the tissue resident leukocytes (mast cells, macrophages and lymphocytes). These local leukocytes are mainly involved in the local tissue function, homeostasis and immune surveillance, and in the presence of a foreign body they may release cytokines and chemokines that drive the recruitment of neutrophils (polymorphonuclear leukocytes) and inflammatory monocytes from the blood stream (Franz et al., 2011). 

Granulocytes (polymorphonuclear leukocytes) Neutrophils Eosinophils Basophils/mast cells"... 

The cells of the immune system are formed from pluripotent stem cells produced in the bone marrow. These stem cells undergo a sequence of cellular differentiations to form B lymphocytes, T lymphocytes, erythrocytes, polymorphonuclear leukocytes, monocytes, macrophages, and mast cells. 

Gold alters the morphology and functional capabilities of human macrophages—possibly its major mode of action. As a result, monocyte chemotactic factor-1, interleukin-8, interleukin-IB production, and vascular endothelial growth factor are all inhibited. Intramuscular gold compounds also alter lysosomal enzyme activity, reduce histamine release from mast cells, inactivate the first component of complement, and suppress the phagocytic activities of polymorphonuclear leukocytes. Auranofin also inhibits release of prostaglandin E2 and leukotriene B4. 

Nedocromil was developed as a result of research for compounds to control asthma. Its activity has been studied in vitro in a variety of inflammatory cells, including mast cells, eosinophils, and polymorphonuclear leukocytes. Nedocromil appears to be more potent than cromolyn in its ability to inhibit immimologic release of mast cell mediators. It can also modify the actions of eosinophils, neutrophils, monocytes, macrophages, and platelets. Pharmacokinetic studies indicate that ocular penetration of nedocromil is slow, and clearance from the eye is relatively rapid. Nedocromil differs from the other mast cell stabilizers in that it is effective within 15 to 30 minutes. 

Specifically, the giant papillae found in VKC consist of dense fibrous tissue (connective tissue hyperplasia) as well as eosinophils, mast cells, basophils, polymorphonuclear leukocytes, lymphocytes, and macrophages. Mucous discharge contains eosinophils. Trantas dots, which appear as elevated white opacities at the limbus, contain eosinophils and epithelial cells. 

These external neural influences on intestinal motility are common targets for prokinetic drugs, but events within the bowel can have important effects on intestinal motility and cause the bowel to be refractory to traditional prokinetic therapy. Release of cytokines from activated inflammatory cells is probably an important feature of ileus in many cases. Ileus secondary to reperfusion injury is an anticipated response in horses with small intestinal obstruction. However, even apparently mild intestinal injury can initiate cellular responses that lead to impaired motility. Mild intestinal insult by gentle surgical manipulation activated adhesion molecules on leukocytes and increased the expression of P-selectin and intercellular adhesion molecule 1 on endothelial cells within the vasculature of the muscularis layer of the intestine (Kalff et al 1999). Surgical manipulation of the rodent small intestine resulted in substantial extravasation of leukocytes into the intestinal muscularis, consisting mainly of polymorphonuclear neutrophils, monocytes and mast cells and lasting for days. This cellular inflammatory response within the intestinal muscularis externa was associated with a marked decrease in jejunal circular muscle activity (Kalff et al 1998). 

Figure 1 Neither anti-IgE nor mast cell deficiency alters BAL cellular composition. N as per Table 1. Mast cell-deficient (W/Wv) mice and wild-type control mice (WT) were sham injected or sensitized with 10 (xg ovalbumin (OVA) IP and 0.75 mg of ALUM on day 0. Starting on day 14 through day 21, all mice received a 30-minute inhalation challenge of aerosolized 1% OVA delivered by a DeVilbiss ultrasonic nebulizer. Antibody-pretreated mice were injected (200 (xg sc) with anti-IgE or an isotype control antibody on days -21, — 14, —1, 0, 7, 14, and 18. On days 14 through 21, mice also received daily inhalations of anti-IgE or control antibody (12 mg aerosolized to completion, deposited lung dose 2 Xg/mouse). Inhalation anti-IgE treatment occurred 1 hour prior to OVA inhalation challenge, p < 0.0001 for overall difference between groups by ANOVA. Only differences between nonsensitized and sensitized groups different by subtest (p < 0.0001). Data are mean standard deviation. PMN, polymorphonuclear leukocyte.

---