Biomedical subjects

Ritu Kumar

Publications and source records attributed to Ritu Kumar.

5 recordsLinked to original sources

PubMed2006

Age-related accumulation of a novel CD44 + CD25lowgammadelta T-cell population in hematopoietic organs of the mouse.

We discovered a novel population of gammadelta T cells in the mouse that accumulates with age in hematopoietic organs, but not in epithelia. These cells are CD25low (an unusual phenotype for gammadelta T cells in the mouse); express higher levels of TCRgammadelta and CD44 than do CD25- gammadelta T cells; mainly express Vgamma2, Vgamma3, and Vgamma4 chains; and are largely quiescent. A very similar cell population appears in the late stages of fetal thymus organ cultures, suggesting that the accumulation of CD44 + CD25lowTCRgammadelta + cells is a response to stress induced by aging in vivo or by culture in vitro. The precursors of CD44 + CD25lowTCRgammadelta + cells are generated during fetal or very young adult life, as this population was undetectable in aged recipients of bone marrow from old or young donors. CD44 + CD25lowTCRgammadelta + cells may be a biomarker of aging, but could also play a role in the inflammatory changes that accompany aging.

Aging↗

PubMed2005

Transforming growth factor-beta2 is involved in quantitative genetic variation in thymic involution.

The mechanisms regulating thymic involution are unclear. In inbred mouse strains the rate of thymic involution and the function of the hematopoietic stem cell (HSC) compartment are subject to quantitative genetic variation. We have shown previously that transforming growth factor-beta2 (TGF-beta2) is a genetically determined positive regulator of HSCs. Here, we demonstrate that genetic variation in the rate of thymic involution correlates with genetic variation in the responsiveness of hematopoietic stem and progenitor cells to TGF-beta2. Corroborating these correlations, thymic cellularity and peripheral naive T-cell frequency were higher in old Tgfb2+/- mice than in wild-type littermates. The frequency of early T-cell precursors was increased in Tgfb2+/- mice, suggesting that TGF-beta2 affects the earliest stages of T-cell development in old mice. Reciprocal transplantation experiments indicated that TGF-beta2 expressed both in the (micro)environment and in the hematopoietic system can accelerate thymic involution; however, the age of the stem cells appeared irrelevant. Thus, although thymic involution is largely determined by the aged environment, TGF-beta2 plays a major modulatory role that is subject to genetic variation and is possibly mediated through its regulatory effects on early hematopoiesis.

Aging↗

PubMed2004

Gut-inhabiting bacterium Oxalobacter formigenes: role in calcium oxalate urolithiasis.

Oxalate plays a crucial role in the formation of most renal stones. Oxalate is a common constituent of most diets and a byproduct of metabolism, and if it is not sufficiently degraded, it may accumulate. In humans, gut bacteria degrade 70 to 100 mg of oxalate per day. Oxalobacter formigenes is a gram-negative, obligately anaerobic, rod-shaped bacterium with an absolute requirement for oxalate. Although not present in the gut at birth, it quickly colonizes most children, and there is epidemiologic evidence that its absence is a risk factor in calcium oxalate stone formation. We review the metabolism, genetics, and identification of this organism and its possible therapeutic role in recurrent stone-forming patients.

Animals↗

PubMed2004

Septic arthritis caused by Chryseobacterium meningosepticum in an elbow joint prosthesis.

Chryseobacterium meningosepticum is a Gram-negative bacillus historically associated with meningitis and sepsis in premature neonates. Clinicians should suspect this organism when Gram-negative bacilli are seen on Gram-stain and culture, particularly in immunocompromised patients, and in cases of disrupted host tissue integrity. We report the first case of septic arthritis due to this organism.

Arthritis, Infectious↗

PubMed2004

Infrequency of colonization with Oxalobacter formigenes in inflammatory bowel disease: possible role in renal stone formation.

BACKGROUND AND AIM: Calcium oxalate renal stones (RS) and hyperoxaluria are common in patients with inflammatory bowel disease (IBD). The absence of intestinal oxalate degrading bacteria, Oxalobacter formigenes, may cause hyperoxaluria in IBD. The aim of the present study was to examine: (i) the colonization of O. formigenes in patients with IBD and controls and to correlate its presence with urinary oxalate excretion; and (ii) urinary analytes contributing to RS in IBD. METHODS: Stool samples were studied for O. formigenes using polymerase chain reaction and Southern blotting in patients with IBD (n = 48: ulcerative colitis, 37; Crohn's disease, 11), RS (n = 87) and healthy subjects that were used as controls (n = 48). Levels of urinary oxalate, citrate, calcium, magnesium, creatinine and uric acid were estimated spectrophotometrically in each patient and in 13 controls for 24 h. RESULTS: Five of the 48 (10.4%) patients with IBD had RS. Five of the 48 (10.4%) patients with IBD, 25 of the 87 (29%) with RS and 27 of the 48 (56%) controls were colonized with O. formigenes (P < 0.001 for RS vs controls and P = 0.01 for RS vs IBD). Patients without O. formigenes had higher urinary oxalate than those with it (IBD, median 0.48 [range 0.11-2.09]vs 0.43 [range 0.16-1.10] mmol/24 h, P = NS; RS, median 0.59 mmol/24 h, range 0.14-1.90 vs 0.44 mmol/24 h, range 0.23-0.97; P = 0.008, Mann-Whitney U-test). Median excretion of oxalate was higher in IBD and RS than in controls (0.47 [0.11-2.09], 0.56 [0.14-1.9] and 0.41 [0.21-0.62] mmol/24 h; P < 0.01), respectively. Median calcium was also higher in IBD and RS than in controls (6.50 [1.38-21.00], 6.78 [1.55-20.30] and 4.99 [1.47-9.60] mmol/24 h; P < 0.05, Kruskal-Wallis H-test), respectively. Median urinary magnesium was higher in IBD than in RS and controls (4.57 [1.50-12.30], 3.60 [0.90-6.35] and 2.49 [0.74-4.80]; P < 0.001, Kruskal-Wallis H-test), respectively. Urinary citrate excretion was comparable in IBD, RS and controls. CONCLUSIONS: Patients with IBD and RS rarely have O. formigenes in their stools as compared with controls; this may contribute to hyperoxaluria in IBD. Hyperoxaluria and hypercalciuria may contribute to RS in patients with IBD. Hypermagnesuria in patients with IBD may protect them from RS.

Adolescent↗