Bartonella henselae Infection in Sickle Cell Disease Mice Is Associated with Hyperalgesia.

BACKGROUND: Sickle cell disease (SCD) is the most prevalent hematologic genetic disorder. Acute vaso-occlusive painful crisis is the hallmark of the disease and may be related to subclinical infections. Bartonellosis, a rare and neglected infection, is caused by Bartonella spp., which can be found in donated blood. These bacteria cause intraerythrocytic and endothelial infection and pain, all of which occur in SCD. It is likely that this infection is transmitted to SCD patients during transfusion from donated blood, leading to pain. We, therefore, evaluated whether Bartonella henselae infection would cause hyperalgesia in mice with SCD. MATERIALS AND METHODS: SCD mice were generated by transplantation of nucleated bone marrow cells harvested from transgenic Berkeley sickle mice into 2-month-old irradiated C57BL/6 mice. We infected four SCD mice by intraperitoneal inoculation with B. henselae, and inoculated four other mice with the same volume of saline. Mechanical hyperalgesia was determined using von Frey monofilaments by two blinded observers. Thereafter, the animals were anesthetized and euthanized to collect blood, liver, and spleen samples to seek B. henselae infection by PCR. FINDINGS: We confirmed the experimental infection in all animals by PCR. Tremors and mechanical hypersensitivity were demonstrated by SCD mice infected with B. henselae infection but not in those receiving saline. CONCLUSION: B. henselae infection may be related to pain and other symptoms in SCD.

Granuloma Faciale and Eosinophilic Angiocentric Fibrosis: Similar Entities in Different Anatomic Sites.

BACKGROUND: Eosinophilic angiocentric fibrosis (EAF) and granuloma faciale (GF) share several histopathologic features, including eosinophil-rich inflammation, microangiitis, and progressive fibrosis. Concurrent presentation of EAF and GF suggests a pathogenetic link between them. OBJECTIVES: To identify histologic findings that tell them apart and construe the pathogenetic mechanisms behind each morphologic variable, 14 immunohistochemical markers were used to study the cells subpopulations in 14 cases of GF and 3 cases of EAF. MATERIALS AND METHODS: The lesions were classified according to their stage of development. The antibodies studied were: CD4, Foxp3, CD8, granzymes A and B, perforin, granulysin, CD20, CD56, CD68, ICAM-1, CD34, CD105, and 1A4. RESULTS: The intensity of the sclerotic response and the density of 1A4-immunostained cells were significantly higher in EAF. In both diseases, CD68 cells were the most numerous, followed by CD20, CD8, and CD4 cells. About 30% of cells expressed ICAM-1. Among cells with cytotoxic granules, granulysin-positive cells were the most frequent. CONCLUSIONS: Differences between GF and EAF were found to be mostly like due to anatomic site (usually skin of the face vs. sinonasal cavity) and stage of the disease development (usually earlier in cutaneous lesions because of their visibility). Innate and adaptive immunity, including B cells, T cells, and cytotoxic granules have a role in their pathogenesis.

Non-invasive method distinguishes chronic telogen effluvium from mild female pattern hair loss: clinicopathological correlation.

BACKGROUND: The distinction between chronic telogen effluvium (CTE) and female pattern hair loss (FPHL) is important because of their different prognosis and treatment. Non-invasive methods have been described to be useful in differentiating FPHL from CTE. This prospective study investigated the use of the washing method to differentiate CTE from mild FPHL. METHODS: Twenty patients with CTE and 17 with FPHL were recruited and followed for 18 months. The diagnosis was established through clinical, laboratory, and histological studies. The patients were asked to abstain from washing their hair for 5 days and then shampoo and collect all hair shed in the process. Hair shafts were then counted and divided into two groups: up to 3 cm in length or longer. RESULTS: In the CTE group, the mean hair count was high (438), and in all cases, <10% were short. In patients with FPHL, the mean count was not as high (215) and in only one patient, short hairs comprised <10% of the total. The greater the number of long hairs, the higher was the density of terminal follicles seen histologically. The CTE group presented a greater number of patients with serum iron values <70 µg/dl. Ferritin levels ranged from 6.98 to 128.33, average of 66.65 (CTE), and 16.5-304.8, average of 114.97 ng/ml (FPHL), but no significant differences were found. CONCLUSION: The washing test can be useful to avoid biopsy procedures. Iron serum levels are possibly an additional parameter that may improve CTE diagnosis if combined with an earlier test.

Perforin and granzyme B expression in oral and cutaneous lichen planus - a comparative study.

BACKGROUND: Although cutaneous and oral lichen planus (LP) share similar histopathological features, oral LP often follows a recalcitrant course while LP skin lesions tend to be self-limiting. Apoptosis, mediated by cytotoxic T-cells in LP, may be triggered by the release of molecules such as perforin and granzyme B. As variation in clinical behavior can reflect differences in LP immune expression, we studied the role of those cytotoxic molecules in oral and cutaneous LP. METHODS: We analyzed 16 cases of cutaneous LP and 29 of oral LP. The sections were studied on hematoxylin and eosin, CD4, CD8, perforin and granzyme B staining. RESULTS: The mean number of immunostained cells expressing each cytotoxic molecule was significantly higher in oral LP than in cutaneous LP. A higher number of single necrotic keratinocytes (apoptotic bodies) was found in oral LP lesions when compared to cutaneous LP. Only in oral LP lesions, a higher number of CD4-positive cells was found in active lesions when compared to regressive lesions. CONCLUSIONS: Our results confirm increased expression of granzyme B and perforin in oral LP lesions as compared to cutaneous LP. The increased expression suggests a relationship with the clinical behavior of the disease.