The Role of ICAM1 Gene in the Improvement or Spreading Wounds Caused Leishmania major

Abstract

Introduction: Leishmaniasis is a common infectious zoonosis disease, which is caused by
different species of Leishmania genus. The disease is transmitted by sandflies, which infects
mononuclear phagocytes in the human host of Leishmania as an intracellular parasite.
Depending on the type of parasite and host immune response, the disease will have different
clinical manifestations so that the symptoms subclinical infections and self-healing
cutaneous occlusion, diffuse and progressive skin occlusion, and mucous membranes, and the
entire reticuloendothelial system (1) vary. The main response of the body to resist this infection
is cell-mediated immunity. The cellular immune system operates with two branches, one of
them is the increase of Th1 that provides protection and the other is the increase of Th2 that
causes the disease to deteriorate. In this type of immunity, the Th1 cells and the resulting
cytokines play a major role. In this study, the production level of this protein was evaluated in
patients with leishmaniasis and control group in order to examine the role of ICAM1 cell surface
protein in the process of improving or spreading wounds caused by Leishmania major.
Method: The study was performed on 44 patients who had previously been diagnosed with
Leishmania Major by sampling from the wound and carrying out PCR test. In Addition, 10cc
blood was taken from 25 health people. The samples were isolated and cultured using the
Ficclean gradient method. Then, RNA was isolated from them in two steps before and after
induction with PHA, and converted to cDNA. The ICAM1 gene expression rate of RTPCR was
measured and compared in both patient and control groups.
Findings: 44 patients were evaluated, 64% of which were males and 36% were females. The
average age of these individuals was 37.6 years old. The highest wound rates were observed in
people’s hands. The difference in expression of ICAM1 gene before and after induction with
PHA was significant in patients with cutaneous leishmaniasis compared to the control group by
Mann-Whitney test.
Conclusion: The current study expresses that immunity in leishmaniasis is dependent on
induction of the immune system and the presence of multiple wounds in the body causes faster
and more severe immune responses and stronger immunity to the disease. This study also
describes the role of Th1 in dermatological leishmaniasis. Accordingly, the expression of the
ICAM1 gene in people with cutaneous leishmaniasis would indicate an increase in the activity of
neutrophils in the infection site and an increase in inflammation, which can also contribute to
the spread of Th1 immune response, and can also lead to parasite limitation, by increasing
inflammation