Jorge Lobo\'s disease (JLD) and lepromatous leprosy (LL) share several clinical, histological and immunological features, especially a deficiency in the cellular immune response. Macrophages participate in innate and adaptive inflammatory immune responses, as well as in tissue regeneration and repair. Macrophage function deficiency results in maintenance of diseases. M1 macrophages produce pro-inflammatory mediators and M2 produce anti-inflammatory cytokines. To better understand JLD and LL pathogenesis, we studied the immunophenotype profile of macrophage subtypes in 52 JLD skin lesions, in comparison with 16 LL samples, using a panmacrophage (CD68) antibody and selective immunohistochemical markers for M1 (iNOS) and M2 (CD163, CD204) responses, HAM56 (resident/fixed macrophage) and MAC 387 (recently infiltrating macrophage) antibodies. We found no differences between the groups regarding the density of the CD163, CD204, MAC387+ immunostained cells, including iNOS, considered a M1 marker. But HAM56+ cell density was higher in LL samples. By comparing the M2 and M1 immunomarkers in each disease separately, some other differences were found. Our results reinforce a higher M2 response in JLD and LL patients, depicting predominant production of anti-inflammatory cytokines, but also some distinction in degree of macrophage activation. Significant amounts of iNOS + macrophages take part in the immune milieu of both LL and JLD samples, displaying impaired microbicidal activity, like alternatively activated M2 cells.

BACKGROUND:  Intracranial aneurysms are more commonly associated with inflammation as a cause of their development, progression, and rupture. Macrophages and other cells can express the CD68 antigen. The aim of this study was to assess the CD68 antigen levels in cerebral aneurysm (CA) patients compared to a control group at a referral center in Iran.
METHODS:  A case-control investigation was undertaken on 88 individuals (44 of whom were cases and 44 were controls). Individuals with CA as the case group consisted of 28 ruptured and 16 unruptured subgroups. Clinical, radiographic, and CD68 levels were evaluated and registered.
RESULTS:  The average age of the participants was 49 years. Males comprised 43.2% of the patients, while 56.8% were females (p = 0.002). There was a statistically significant difference in the CD68 levels between the two groups. There was no significant difference (p = 0.42) between the ruptured and unruptured subgroups (23.66 and 20.47, respectively) in this comparison. No significant correlation was seen between the patients\' CD68 and Glasgow Coma Scale (GCS) levels and their aneurysm diameter (p = 0.74 and 0.45, respectively). A link between CD68 levels and age was found, but it was not statistically significant (r = 0.44 and p = 0.002).
CONCLUSIONS:  A possible involvement of CD68 as an inflammatory agent in the development of CAs but not in aneurysm rupture has been suggested. Inflammation and CD68 were positively associated with age. The CD68 antigen should be studied further in population-based cohort studies.