Inflammatory cell infiltration

Figure 17. Inflammatory cell infiltrate in a muscle biopsy from a patient with dermatomyositis note compact nature of infiltrate and perivascular location.

The histopathological features of PM may be radically different from those of JDM and ADM. There is little, if any, evidence of involvement of the micro vasculature and the muscle necrosis which occurs appears to be the direct result of targeting of individual muscle fibers. In the dermatomyositis syndromes, antibody-dependent humoral mechanisms are predominant and B-lymphocytes are seen to be the most abundant cell type in almost all JDM cases and a substantial proportion of ADM cases. In contrast, most muscle biopsies from PM patients show evidence of inflammation in which TS (cytotoxic) lymphocytes predominate (Figure 20). Moreover, the distribution of inflammatory cell infiltrates tends to be different. Instead of the mainly perifascicular location of lymphocytes in JDM/ADM, there... 

Jaber, J.R. et al., Immunophenotypic characterization of hepatic inflammatory cell infiltrates in common dolphins (Delphinus delphis), J. Comp. Pathol., 129, 226, 2003. 

Respiratory hypersensitivity is an adverse reaction in the respiratory tract driven by immune mechanisms such as IgE antibody mediated allergic responses. Other less well understood mechanisms that have an immune component are also involved in respiratory hypersensitivity. OA is one outcome of respiratory hypersensitivity. Respiratory hypersensitivity and OA to proteins are primarily mediated by IgE antibody with subsequent inflammatory cell infiltrates. This same mechanism is responsible for OA to specific LMW chemicals such as the acid anhydrides and platinum salts. However, the role for IgE mediated responses in OA to other LMW chemicals such as the isocyanates and plicatic acid is poorly defined and other mechanisms may be responsible. 

Another study in Fischer rats demonstrated that MSCs do not elicit an immune response after transplantation in immunocompetent recipients. Syngeneic Fischer MSCs or allogeneic ACI MSCs were implanted via an osteoconductive matrix into the bilateral femoral gap of Fischer rats who were then sacrificed at 3, 6 and 12 weeks post-implantation (n = 4 per time point). Histological analysis showed there was no difference between the syngeneic or allogeneic implants. Allogeneic implants did not induce significant inflammatory cell infiltration or stimulate alloreactive T-cell responses [656702]. 

Londono, D.P., Alvarez, J.I., Trujillo, J., Jaramillo, M.M. and Restrepo, B.l. (2002) The inflammatory cell infiltrates in porcine cysticercosis immunohistochemical analysis during various stages of infection. Veterinary Parasitology 109, 249-259. 

Skin damage has been observed in female TF, Carworth mice, New Zealand rabbits, and Large White pigs following the application of 10% aluminum chloride (0.005-0.1 g Al) or aluminum nitrate (0.006-0.013 g Al) for 5 days but not from aluminum sulfate, hydroxide, acetate, or chlorhydrate (Lansdown 1973). The damage consisted of hyperplasia, microabscess formation, dermal inflammatory cell infiltration, and occasional ulceration. These results suggest that the development of adverse dermal effects from exposure to aluminum depends upon its chemical form. 

Vascular intervention results in cellular injury and the release of several mediators of thrombotic and inflammatory processes. Endothelial cell injury results in luminal thrombosis, inflammatory cell infiltration, cellular proliferation, and... 

At three-months, the stenosis was reduced by 20 and 34% in the treatment groups. Histopathology evaluation showed that there were no adverse effects of the drug-loaded stent compared to the controls, and no deleterious phenomenon could be attributed to the drug tested. The intensity of fibrosis, hemorrhages, and inflammatory cell infiltration was not significantly different from the control group at three months,... 

The five-day, one-, and three-month preclinical data are available for PC-stents loaded with the CTD of batimastat. Histological analysis showed that the degree of fibrosis, hemorrhages, and inflammatory cell infiltration was not significantly different between the control and CTD stents at all three time points. Five-day and one-month data are available for stents containing greater than three times the CTD. Taken together, these studies demonstrate that the Biod/VY s/o Batimastat Stent is well tolerated in appropriate animal... 

One of the main reasons for interest in chemokines is the ease with which their expression can be documented in physiological settings involving leukocyte trafficking or in diseases characterized by inflammatory cell infiltration. In the case of most ELR-containing CXC chemokines, their ability to attract neutrophils in vitro is paralleled by a similar activity when injected in vivo (1-3). However, in the case of non-ELR CXC and most CC chemokines, injection in vivo has resulted in disparate and inconsistent reports of activity (4-6). Thus, in order to be able to infer anything about the function of chemokines in normal physiology or disease, it must be demonstrated that their in vitro activities accurately predict their in vivo activities. 

Casillas and Babin, unpublished). Finally, inflammatory cell infiltration, which may occur about a day after exposure, may also play a role in delaying SM wound healing (Maumenee and Schloz, 1948). The sheer number of potential target areas in a multilayered, multicell organ that may be affected by sulfur mustard make the task of determining SM s exact mechanism of action quite difficult. 

FIGURE 41.4. Biphasic inflammatory response in the MEVM hematoxylin and eosin stained paraffin sections of mouse ears with (right, 168h post-exposure) and without (left, carrier solvent, alone). Note the edema in the treated ear. The 168h post-SM sample had a very large inflammatory cell infiltration (purple nuclei of thousands of infiltrating cells is apparent). 

Unlike the more commonly encoimtered episcleritis, inflammation of the sclera is relatively rare, painfiil, and capable of extensive and permanent tissue and visual destruction. Scleritis is characterized by an immime-mediated vasculitis and inflammatory cell infiltration of the sclera and episclera. Scleritis usually occurs in the fiaurth to sixth decades of life but can be seen at any age. Peak incidence fi>r men is in the fiaurth decade, whereas there are two peaks for women the third and sixth decades. Diffuse scleritis shows a 1 1 distribution, whereas the other forms, particularly necrotizing and posterior scleritis, show a female predilection. Scleritis presents bilaterally about 50% of the time, and unilateral presentations usually... 

The pathophysiology of scleritis is complex and not fully understood.The main dysfunction is thought to be the deposition of immime complexes in the vasculature of the sclera and episclera, creating a vasculitis. This leads to edema and inflammatory cell infiltration of the sclera and episclera, which in turn cause disorganization and destruction of the collagen lamellae. However, not all presentations of scleritis demonstrate the same pathology. 

An increase in the total numbers of T-Iymphocytes is observed in lung parenchyma as well as in peripheral and central airways of patients with COPD a greater increase is observed in CD8 than CD4+ cells (6, 24). A correlation is observed between the numbers of T-cells and the amount of alveolar destruction and the severity of airflow obstruction. Furthermore, the oifly significant difference in the inflammatory cell infiltrate in asymptomatic smokers and smokers with COPD is an increase in T-cells, maiifly CD8+, in patients with COPD. An increase in the absolute number of CD4+ T-cells, albeit in smaller numbers, is evidenced in the airways of smokers with COPD, and these cells express activated STAT-4, which is a transcription factor that is essential for activation and commitment of the Thl lineage, and IFN-y. 

Inflammatory cells infiltrating postischemic tissue are considered to contribute to disability after cerebral ischemia [5,8,17]. Identification of factors involved in the selective recruitment and accumulation of inflammatory cells into ischemic brain tissue and the mechanisms behind the entry of leukocytes through the blood-brain barrier into sites of ischemia are not completely understood [5,8]. Locally produced proinflammatory cytokines such as TNF-a, IL-1 P, and IL-6 initiate the inflammatory process. TNF-a and IL-1 P mRNA elevate in the brain after experimental middle cerebral artery occlusion [5,51,81]. While, IL-1 p and TNF-a play a major role in promoting adhesion between endothelial cells and leukocytes, they are poor attractants for polymorphonuclear leukocytes and monocytes [7]. Astrocytes and endothelial cells can respond in vitro to such proinflammatory cytokines with enhanced expression of chemokines, which results in the influx of leukocytes to areas of inflammation [5,8,103]. 

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