Immunochemistry & Immunopathology

Biopolymer researchers have advanced new strategies to improve the properties of wound dressings over the last decade which is becoming one of the most swiftly growing fields in the biomedical and pharmacy. The advantages of these biopolymers (particularly chitosan) is that, they can be easily processed into different forms which needs to be for different biomedical applications. Chitosan is the well-known natural biopolymer which is safe to be use, biocompatible and biodegradable in nature. This review provides an outline of the chitosan properties and its biomedical properties toward applications in anti-inflammatory and wound caring management.

Inflammation is one of the important responses elicited by organisms to counteract obnoxious stimuli. However, continuous inflammation has been responsible for the induction of several diseases. Therefore, it is essential to combat excess inflammation by devising countermeasures to neutralize excess inflammation. The present study was undertaken to investigate the analgesic and anti-inflammatory activities of hesperidin, a citrus flavonoid in mice using standard procedures employed for these activities including hotplate, acetic acid, tail immersion, xylene and formalin-induced edema tests. Treatment of mice with different doses of hesperidin revealed that hesperidin induced analgesic and anti-inflammatory activities in a dose dependent manner as indicated by pain inhibition and reduced inflammation. The maximum effect was observed for 300 mg/kg b. wt. hesperidin. Our study demonstrates that hesperidin has analgesic as well as anti-inflammatory action.

Background: Analytical results estimating Uncertainty of Measurement (MU) signifies the confidence level of the concerned assay. Enzyme-linked immunosorbent assay (ELISA) is an extensively used important tool for infectious disease sero-diagnosis, nevertheless, MU for ELISA result is not reported since procedure of MU estimation is hardly available. International Organization for Standardization (ISO) provides the Guide to the Expression of Uncertainty in Measurement (GUM) describing set of guidelines, however no detailed procedures or instructions for evaluating specific measurement processes is described. This article aims step by step procedure for MU estimation in a serology laboratory by describing the potential sources of uncertainty during each step of ELISA.

Methods: HIV sample was tested by commercial ELISA following routine procedure. Uncertainty was estimated by specification of measurand, identification of uncertainty sources, quantification of values attributed to the sources of uncertainty and calculation of the combined standard uncertainty following GUM by converting all the standard uncertainties of ELISA into dimensionless relative standard uncertainties. The combined standard uncertainty was calculated using the propagation principle

Results: Uncertainty arising from systematic error (RSD 0.10966) and routine analytical imprecision (RSD 0.04938) were considered as the sources of uncertainty contributing to the total MU of this routine qualitative diagnostic method. Analysis of the data revealed that results obtained for the relative expanded uncertainty U_rel was 24% with 95% confidence level (k=2).

Conclusion: Quantification of uncertainty by combining systematic error and analytical imprecision seems a feasible method of MU for ELISA. The estimated MU reflects the extent of variation for the cut-off absorbance for equivocal outcome of the qualitative interpretation.

It has been calculated that metastasizing lung cancers are numbered in millions. It has also been argued that lymph nodes occupy the status of organs in cancer metastasis. Accordingly, both the tissues now generally regarded as organs as well as lymph nodes, which are of that same status, should all be haphazardly showered by circulating cancer cells. On the contrary, these two sets of organs exhibit very conspicuous diversity in their colonization patterns. Thus, the better known organs generally exhibit scattered secondaries all over the body while the lymph nodes are selectively affected. Thus, in the words of Willis, a foremost cancer authority, lung cancers “often” exhibit discrete deposits in the abdominal lymph nodes, “these diminishing in centrifugal order.” Indeed, such an order is not known as regards, say, the liver, adrenal gland, kidney and ovaries. Therefore, is Nature showing signals which ought to be decoded? Here, I argue that this is possible. Moreover, the welcome expectation is that such a study of lung cancer can usher in an immunological breakthrough which may point to target therapy and thereby conduce to cancer cure.

Aim: To demonstrate the presence of differentiated cells in ovarian carcinomatosis nodules after chemotherapy.

Patient and method: A patient of 85 years, who presented a pelvic mass of 10 cm. The anatomo-pathological study was performed on the biopsies (before treatment) and post operational samples (after treatment by Carbotaxol). Histological samples were analyzed with ovarian cancer markers for diagnosis. The immune cells (CD3, CD4, CD8 and CD20) and neural markers such as anti: neurofilament (NF), neural cell adhesion molecules NCAM (CD56), chromogranin A, neuronal specific enolase (NSE), S100 protein and synaptophysine were used for demonstrating the neuronal differentiation tendencies of carcinomatosis cells. Proliferation activities were studied by using proliferative index and Ki67 antibody.

Results: The histological result of biopsies of bilateral ovarian carcinomatosis showed the poorly differentiated monomorphic cell serous carcinoma (cytokeratin+, estrogen receptor+, protein S100+, anti-wilms tumor-1+ with proliferative index (31%) and high Ki67 marker (45%). Semi-quantitative histological evaluations of post operational samples presented two cellular quotas. One was composed of monomorphic cells with high proliferative index (19%) and ki67 marker (30%). In another quota, large size polymorphic cells with no proliferative index and Ki67 marker were distinguished. Before treatment, all neuronal markers except NSE and S100 protein were found negative in primary tumors. In the proliferative zone of post-operative samples, NSE and S100 protein markers persist with any other neuronal markers. These zones were highly infiltrated by CD3, CD4 and CD20 immune cells. In contrast, in degenerative non-proliferative zone, all primary tumor markers except Ki67, all neuronal markers except synaptophysine, and dramatically decreased infiltrated immune cells.

Conclusion: These results are in favors of differentiation of poorly differentiated ovarian cancer cells with high proliferative index to other tissue with no proliferation potential. Targeting of differentiation of cancer cells by differencing inductors may be a new way for cancer therapy.

In atopic dermatitis, we have recently shown the innate immune system is activated by biofilm-forming staphylococci that occlude sweat ducts. Toll-like receptor 2 (TLR 2) is activated and moves from its epidermal control location in the basal zone to the proximal stratum corneum (surrounding the occluded duct). There it likely initiates the MyD88 and the PAR 2 pathways in an effort to inactivate the staphylococci; these efforts are fruitless because of the biofilms and lead to the prime pathological finding of spongiosis and to the prime symptom of pruritus which leads to the disease. If the pruritus is intense enough to cause excoriations severe enough to disrupt the epidermis, the involvement of the dermis likely causes the activation of the adaptive immune system leading to the documented appearance of IL 31, another even more potent pruritogen.
We have also shown that the innate system is involved in psoriasis, again with TLR 2. This time it was present in the dilated upper dermal capillaries; TLR 2 has been shown to lead to TNFa, IL 12/23, and IL 17 which have all been shown to be involved in the production of psoriatic lesions. In this instance, the streptococcus is most likely the organism involved; it is not recoverable because it internalizes or makes biofilms, so TLR 2 instead of combating the bacterium attacks host cells. Anti-streptococcal IgG is markedly elevated in plaque psoriasis in one half the patients; it is of interest to postulate these patients were those who would develop the systemic findings of arthritis, uveitis, and the metabolic syndrome which develop in 40% of patients.
In chronic arthritis, Lyme disease, and Alzheimer’s disease where the disease has been shown to be caused by Borrelia and dental spirochetes, TLR 2 is activated because of the presence of the microbes and their biofilms and leads to the chronic course noted in osteoarthritis, Lyme neuroborreliosis and Alzheimer’s disease. When the adaptive immune system is involved, as in rheumatoid arthritis and after a stroke, it is curious that the disease occurs more rapidly and is much more destructive.