Contact Details:

m.bombardieri@qmul.ac.uk

 

Dr Bombardieri graduated in July 1999 in Medicine and Surgery at Catholic University of Rome with 110/110 (cum laude) with a thesis on antiendothelial cell antibodies in neuropsychiatric lupus. He joined in 2000 the group of Prof Valesini at University of Rome “La Sapienza” where he was awarded the title of specialist in Rheumatology in November 2003. Since October 2002 he joined Prof Pitzalis’ group at Kings College London first as an Honorary Research Fellow and then, from October 2003, as a PhD student in Experimental Rheumatology. In July 2005 Dr Bombardieri was awarded a Clinical Research Fellowship from the arthritis research campaign (arc) for a project aimed to investigate the role of IL-18 in the pathogenesis of Sjögren’s syndrome. Following completion of his PhD in 2007 he relocated to the William Harvey Research Institute at Queen Mary University of London as part of the new Centre for Experimental Medicine and Rheumatology. He is currently an arc Clinician Scientist (2008-2012) with a project investigating the cellular and molecular mechanisms of B cell activation in autoimmune rheumatic diseases.

 

Current research interests

 

Dr Bombardieri has a long standing research interest in the pathogenesis of chronic inflammatory/autimmune disorders, with particular focus on the role of inflammatory cytokines and chemokines and of new autoantibody specificities in rheumatoid arthritis (RA), systemic lupus erythematosus, antiphospholipid syndrome and Sjögren’s syndrome (SS). He is currently working on two main projects: 1) identification of novel cytokines and their pathogenic relevance in patients with and animal models of SS and 2) dissecting the mechanisms regulating B lymphocytes recruitment, activation, proliferation and differentiation in the salivary glands of patients with SS and in the synovium of RA. In addition, Dr Bombardieri is currently investigating the cellular and molecular mechanisms involved in the response/relapse/resistance to B cell depleting agents in SS and RA.

 

 

Key publications

 

• Manzo A, Bombardieri M, Humby F and Pitzalis C. Secondary and ectopic lymphoid tissue responses in rheumatoid arthritis: from inflammation to autoimmunity and tissue damage⁄remodeling. Immunological Reviews (in press).
  
  
• Ciccia F*, Bombardieri M*, Principato A, Giardina A, Tripodo C, Porcasi R, Peralta S, Franco V, Giardina E, Craxi A, Pitzalis C, Triolo G. Overexpression of interleukin-23, but not interleukin-17, as an immunologic signature of subclinical intestinal inflammation in ankylosing spondylitis. Arthritis Rheum. 2009 Apr;60(4):955-65.
  
  
• Conigliaro P, Priori R, Bombardieri M, Alessandri C, Barone F, Pitzalis C, McInnes IB, Valesini G. Lymph node IL-18 expression in adult-onset Still's disease. Ann Rheum Dis. 2009;68:442-3.
  
  
• Humby F*, Bombardieri M*, Manzo A, Blades MC, Kirkham B, Spencer J and Pitzalis C. Ectopic Lymphoid Structures Expressing AID Drive Self Sustained in situ Production of Autoantibodies in Rheumatoid Synovium. PLoS Med. 2009 Jan 13;6(1):e1.
  
  
• Barone F*, Bombardieri M*, Rosado MM, Morgan PR, Challacombe SJ, De Vita S, Carsetti R, Spencer J, Valesini G and Pitzalis C. Differential expression of CXCL13, CCL21 and CXCL12 in parotid glands with Lymphoepithelial proliferation and Mucosal Associated Lymphoid Tissue lymphomas in patients with Sjögren’s syndrome associates with diverse  microenvironments of B cell aggregation and proliferation. (submitted, J Immunol) (*contributed equally)
  
  

• Alessandri C, Sorice M, Bombardieri M, Conigliaro P, Longo A, Garofalo T, Manganelli V, Conti F, Degli Esposti M and Valesini G. Anti-phospholipid reactivity against cardiolipin metabolites occurring during endothelial cell apoptosis. Arthritis Res Ther 2006;8:R180

• Bombardieri M, Barone F, Pittoni V, Alessandri C, Conigliaro P, Blades MC, Priori R, McInnes IB, Valesini G, Pitzalis C. Increased circulating levels and salivary gland expression of Interleukin-18 in patients with Sjogren's syndrome: relationship with autoantibody production and lymphoid organization of the periductal inflammatory infiltrate. Arthritis Res Ther 2004;6:R447-R456
  
  
• Alessandri C, Bombardieri M, Del Papa N, Cinquini M, Magrini L, Tincani A, Valesini G. Decrease of anti-cyclic citrullinated peptide antibodies and rheumatoid factor following anti-TNFa therapy (Infliximab) in Rheumatoid Arthritis is associated with clinical improvement. Ann Rheum Dis 2004;63:1218-1221

• Bombardieri M, Alessandri C, Labbadia G, Iannuccelli C, Carlucci F, Riccieri V, Paoletti V, Valesini G. Role of anti-cyclic citrullinated peptides antibodies in discriminating patients with rheumatoids arthritis froom patients with chronic hepatitis C infection-associated polyarticular involvement. Arthritis Res Ther 2004, 6; R137-R141

•  Pittoni V, Bombardieri M, Spinelli FR, Scrivo R, Alessandri C, Conti F, Spadaro A, Valesini G. Anti-tumour necrosis factor (TNF) alpha treatment of rheumatoid arthritis (infliximab) selectively down regulates the production of interleukin (IL) 18 but not of IL12 and IL13. Ann Rheum Dis. 2002;61:723-5

 

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