Hepatic Campylobacter jejuni infection in patients with Castleman-Kojima disease (idiopathic multicentric Castleman disease with thrombocytopenia, anasarca, fever, reticulin fibrosis, and organomegaly (TAFRO) syndrome).

Castleman-Kojima disease, also known as idiopathic multicentric Castleman disease with TAFRO syndrome (iMCD-TAFRO), is a recently recognized systemic inflammatory disorder with a characteristic series of clinical symptoms, including thrombocytopenia (T), anasarca (A), fever (F), reticulin fibrosis (R), and organomegaly (O). Patients with iMCD-TAFRO often develop severe abdominal pain, elevated alkaline phosphatase levels, and systemic inflammation, but the etiological factors are unknown. To investigate the potential role of bacterial infection in the pathogenesis of iMCD-TAFRO, we performed polymerase chain reaction (PCR) for the bacterial 16S rRNA gene with DNA extracted from liver specimens of three patients with iMCD-TAFRO, four patients with amyotrophic lateral sclerosis, and seven patients with inflammatory conditions. Sequencing of the PCR product showed 99% DNA sequence identity with Campylobacter jejuni in all three patients with iMCD-TAFRO and in two patients with inflammatory conditions. Immunohistochemical and electron microscopy analyses could not identify C. jejuni in patients with iMCD-TAFRO. The findings indicated that C. jejuni infection is not the pathological cause of iMCD-TAFRO; however, this ubiquitous bacterium may play a role in uncontrolled systemic hypercytokinemia, possibly through the development of cross-reactive autoantibodies.

Oral antibiotics reduce body temperature of healthy rabbits in a thermoneutral environment.

Nonabsorbable oral antibiotics, which reduce gut flora, decrease the daytime and night-time body temperatures of rats and mice. We investigated whether oral antibiotics would also lower the body temperature of healthy rabbits. Six rabbits received neomycin sulphate in their drinking water for ten days, and seven rabbits received a mixture of chloramphenicol and dihydroxystreptomycin for six days. Body temperatures, recorded using intra-abdominal radiotelemeters, decreased significantly, by 0.2-0.3 degree C, after three days of antibiotic treatment in both groups of rabbits. The drop in body temperature was transient; after six days body temperatures returned to pre-antibiotic levels. Antibiotic treatment had no effect on either the acrophase or the amplitude of the circadian rhythm in body temperature. Oral antibiotics therefore reduce body temperature of rabbits, without influencing the circadian rhythm in body temperature. Our results are consistent with the hypothesis that an agent arising from intestinal bacteria sustains an elevated body temperature in healthy animals.

Attempts to identify the active factor of reticulin-M by high voltage electrophoresis and by acetone precipitation.

The reticulin-M forte (R forte), an antianaphylactic peptide, extracted from organs rich in RES, previously stimulated with India ink, was analysed after acetone precipitation by paper high voltage electrophoresis. Finally the biological activity remains concentrated in the second, arbitrary group of basic peptides, fractions 1 and 3.

Reticulin-M, an antianaphylactic peptide secreted by reticulo-endothelial system.

I. Moldovan (1923) demonstrated in the blood ultrafiltrate from anaphylactically prepared guinea pigs, which believed to anaphylactic shock, or which were previously injected with coloidal substances as India ink to stimulate the RES, an antianaphylactic principle named Reticulin-M(R). Authors extracted R from organs rich in RES with acetone, established their, peptidic nature and tested it on anaphylactic prepared guinea pig uterine horns in vitro. The peptides were fractioned by high voltage paper electrophoresis. The fractions were cut up in four groups, eluted and tested. The second basic group was identified as active and concentrated by acetone, recipitation. In conclusion several techniques were used to obtain, to test, to isolate and to concentrate R, a natural antianaphylactic peptidic factor, which may be a cytokine.