Samuel J. Black

Samuel J. Black

Professor

Photo of Samuel Black

Office phone: 413-545-2573

Fax: 413-545-6326

Email: sblack [at] vasci [dot] umass [dot] edu

Office location: 427G ISB

Ph.D.: University of Edinburgh,
Postdoctoral Training:
Cologne University, Germany
Stanford University, USA
International Laboratory for Research in Animal Diseases, Kenya

Classes:
ANIML SCI 372 - Animal Diseases

Molecular basis for Control of African Trypanosomiasis and Equine Laminitis

Molecular Basis of Immunity against African trypanosomes (Collaboration with Stefan Magez, Free University of Brussels, Belgium, Terry Pearson , University of Victoria, Canada, and Jan Naessens, ILRI, Kenya) –

Our goal is to identify molecular interactions between mammal hosts and African trypanosomes that affect the development of protective immune responses as well as pathophysiologic processes. African trypanosomes are flagellated protozoa that cause sleeping sickness in people and Nagana in domestic animals. These diseases are fatal if left untreated. The diseases are endemic in the humid and semi-humid zones of Africa affecting a landmass of 10 million km 2 and 36 countries. Trypanosomiasis precludes cattle-based agriculture from much of this area and threatens up to 60 million people, of whom about a half million are presently infected. We are taking three approaches: (i) elucidating the protective responses that develop in Cape buffalo. These trypanosomiasis-resistant bovids co-evolved with African trypanosomes and efficiently suppress trypanosome parasitemia to a cryptic level upon infection. (ii) Elucidating the CD1d-restricted protective immune response that arises in mice that are vaccinated against the GPI anchor of the trypanosome variant surface glycoprotein, or infected with phospholipase C knock-out trypanosomes. (iii) Elucidating the contribution of TNF ” , ADAM 17 (TACE) and TIMP3 to regulation of trypanosome-induced pathology

Control of inflammation in equine laminitis (collaboration with Jim Belknap, Ohio State University School of Veterinary Medicine) –

Our goal is to develop prophylactic therapies against equine laminitis. The digital laminae are composed of extracellular matrix and link the coffin bone of the foot to the hoof wall, thus suspending the horse’s weight within the hoof. Failure of the laminae results in severe lameness and affected horses are often euthanized. Our studies show that failure of the laminae is preceded by local elevated expression of the neutrophil chemoattractant IL-8, followed by recruitment of blood neutrophils which release matrix metalloproteinase 9 and oxygen radicals possibly causing laminar pathology. Current research is directed at further resolving pathophysiologic processes that lead to laminitis including, i) neutrophil and vascular endothelium interactions that result in extravasation of the inflammatory leukocytes, ii) the involvement of elastase, metalloproteinases of the ADAM and ADAM-TS families and their inhibitors (TIMPs) in breakdown of the laminar matrix, iii) the involvement of reactive oxygen and nitrogen species in loss of laminar integrity including fibroblast and basal epithelial cell hemidesmosome number and molecular constituents.

Pawlak E, Wang L, Johnson PJ, Nuovo G, Taye A, Belknap JK, Alfandari D, Black SJ.  2012.  Distribution and processing of a disintegrin and metalloproteinase with thrombospondin motifs-4, aggrecan, versican, and hyaluronan in equine digital laminae.. American journal of veterinary research. 73(7):1035-46.
Goenka R, Guirnalda PD, Black SJ, Baldwin CL.  2012.  B Lymphocytes provide an infection niche for intracellular bacterium Brucella abortus.. J Infect Dis. 206(1):91-8.
Bockstal V, Guirnalda P, Caljon G, Goenka R, Telfer JC, Frenkel D, Radwanska M, Magez S, Black SJ.  2011.  T. brucei infection reduces B lymphopoiesis in bone marrow and truncates compensatory splenic lymphopoiesis through transitional B-cell apoptosis.. PLoS pathogens. 7(6):e1002089.
Black SJ, Guirnalda P, Frenkel D, Haynes C, Bockstal V.  2010.  Induction and regulation of Trypanosoma brucei VSG-specific antibody responses.. Parasitology. 137(14):2041-9.
Coyne MJ, Cousin H, Loftus JP, Johnson PJ, Belknap JK, Gradil CM, Black SJ, Alfandari D.  2009.  Cloning and expression of ADAM-related metalloproteases in equine laminitis.. Veterinary immunology and immunopathology. 129(3-4):231-41.
Loftus JP, Johnson PJ, Belknap JK, Pettigrew A, Black SJ.  2009.  Leukocyte-derived and endogenous matrix metalloproteinases in the lamellae of horses with naturally acquired and experimentally induced laminitis.. Veterinary immunology and immunopathology. 129(3-4):221-30.
Black SJ.  2009.  Extracellular matrix, leukocyte migration and laminitis.. Veterinary immunology and immunopathology. 129(3-4):161-3.
Loftus JP, Black SJ, Pettigrew A, Abrahamsen EJ, Belknap JK.  2007.  Early laminar events involving endothelial activation in horses with black walnut- induced laminitis.. American journal of veterinary research. 68(11):1205-11.
Guirnalda P, Murphy NB, Nolan D, Black SJ.  2007.  Anti-Trypanosoma brucei activity in Cape buffalo serum during the cryptic phase of parasitemia is mediated by antibodies.. International journal for parasitology. 37(12):1391-9.
Loftus JP, Belknap JK, Black SJ.  2006.  Matrix metalloproteinase-9 in laminae of black walnut extract treated horses correlates with neutrophil abundance.. Veterinary immunology and immunopathology. 113(3-4):267-76.
Black SJ, Lunn PD, Yin C, Hwang M, Lenz SD, Belknap JK.  2006.  Leukocyte emigration in the early stages of laminitis.. Veterinary immunology and immunopathology. 109(1-2):161-6.
Kurokawa M, Sato K-ichi, Wu H, He C, Malcuit C, Black SJ, Fukami K, Fissore RA.  2005.  Functional, biochemical, and chromatographic characterization of the complete [Ca2+]i oscillation-inducing activity of porcine sperm.. Developmental biology. 285(2):376-92.
Rogers AN, Welte S, Black SJ, Baldwin CL.  2002.  Partial cDNA sequences of bovine CD72 and CD166/ALCAM, ligands for SRCR-family accessory molecules CD5 and CD6.. Veterinary immunology and immunopathology. 85(3-4):233-9.
Wang J, Van Praagh A, Hamilton E, Wang Q, Zou B, Muranjan M, Murphy NB, Black SJ.  2002.  Serum xanthine oxidase: origin, regulation, and contribution to control of trypanosome parasitemia.. Antioxidants & redox signaling. 4(1):161-78.
Baldwin CL, Sathiyaseelan T, Naiman B, White AM, Brown R, Blumerman S, Rogers A, Black SJ.  2002.  Activation of bovine peripheral blood gammadelta T cells for cell division and IFN-gamma production.. Veterinary immunology and immunopathology. 87(3-4):251-9.
Sathiyaseelan T, Naiman B, Welte S, Machugh N, Black SJ, Baldwin CL.  2002.  Immunological characterization of a gammadelta T-cell stimulatory ligand on autologous monocytes.. Immunology. 105(2):181-9.
Black SJ, Sicard EL, Murphy N, Nolan D.  2001.  Innate and acquired control of trypanosome parasitaemia in Cape buffalo.. International journal for parasitology. 31(5-6):562-5.
Black SJ, Seed JR, Murphy NB.  2001.  Innate and acquired resistance to African trypanosomiasis.. The Journal of parasitology. 87(1):1-9.
Wang Q, Hamilton E, Black SJ.  2000.  Purine requirements for the expression of Cape buffalo serum trypanocidal activity.. Comparative biochemistry and physiology. Toxicology & pharmacology : CBP. 125(1):25-32.
Black SJ, Wang Q, Makadzange T, Li YL, Van Praagh A, Loomis M, Seed JR.  1999.  Anti-Trypanosoma brucei activity of nonprimate zoo sera.. The Journal of parasitology. 85(1):48-53.
Wu H, He CL, Jehn B, Black SJ, Fissore RA.  1998.  Partial characterization of the calcium-releasing activity of porcine sperm cytosolic extracts.. Developmental biology. 203(2):369-81.
Black SJ, Muranjan M, Wang Q.  1997.  Identification of the cape buffalo serum trypanocidal protein: xanthine: oxygen oxidoreductase.. Biochemical Society transactions. 25(3):534S.
Name Phone Office
Frenkel , Deborah 413-545-5561 460 ISB
Zhang , Fengqui Judy 413-545-5561 460 ISB
Former Lab Personnel