Kenshi Yamasaki

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi The molecular pathology of rosacea
    Kenshi Yamasaki
    Division of Dermatology, University of California, San Diego, CA 92161, USA
    J Dermatol Sci 55:77-81. 2009
  2. ncbi Staphylococcus epidermidis antimicrobial delta-toxin (phenol-soluble modulin-gamma) cooperates with host antimicrobial peptides to kill group A Streptococcus
    Anna L Cogen
    Division of Dermatology, University of California San Diego, San Diego, California, United States of America
    PLoS ONE 5:e8557. 2010
  3. ncbi Increased serine protease activity and cathelicidin promotes skin inflammation in rosacea
    Kenshi Yamasaki
    Division of Dermatology, University of California, San Diego, and VA San Diego Health Care System, 3350 La Jolla Village Drive, San Diego, California 92161, USA
    Nat Med 13:975-80. 2007
  4. ncbi TLR2 expression is increased in rosacea and stimulates enhanced serine protease production by keratinocytes
    Kenshi Yamasaki
    Division of Dermatology, Department of Medicine, University of California, San Diego, VA San Diego Health Care System, San Diego, California, USA
    J Invest Dermatol 131:688-97. 2011
  5. ncbi Cathelicidin antimicrobial peptides inhibit hyaluronan-induced cytokine release and modulate chronic allergic dermatitis
    Yasuhide Morioka
    Division of Dermatology, University of California, San Diego, and Veterans Affairs San Diego Health Care System, San Diego, California 92161, USA
    J Immunol 181:3915-22. 2008
  6. ncbi NLRP3/cryopyrin is necessary for interleukin-1beta (IL-1beta) release in response to hyaluronan, an endogenous trigger of inflammation in response to injury
    Kenshi Yamasaki
    Division of Dermatology, University of California, and Veterans Affairs San Diego Health Care System, San Diego, CA 92161, USA
    J Biol Chem 284:12762-71. 2009
  7. ncbi Engagement of CD44 by hyaluronan suppresses TLR4 signaling and the septic response to LPS
    Jun Muto
    Division of Dermatology, University of California, San Diego and VA San Diego Health Care System, San Diego, CA 92161, USA
    Mol Immunol 47:449-56. 2009
  8. ncbi Cathelicidin antimicrobial peptide LL-37 in psoriasis enables keratinocyte reactivity against TLR9 ligands
    Shin Morizane
    Division of Dermatology, Department of Medicine, University of California, San Diego and VA San Diego Healthcare System, San Diego, California, USA
    J Invest Dermatol 132:135-43. 2012
  9. ncbi Selective antimicrobial action is provided by phenol-soluble modulins derived from Staphylococcus epidermidis, a normal resident of the skin
    Anna L Cogen
    Division of Dermatology, Department of Medicine, University of California San Diego, VA San Diego Health Care System, San Diego, California, USA
    J Invest Dermatol 130:192-200. 2010
  10. ncbi Mast cell cathelicidin antimicrobial peptide prevents invasive group A Streptococcus infection of the skin
    Anna Di Nardo
    Department of Medicine, Division of Dermatology, University of California, San Diego and Veteran s Affairs Medical Center San Diego, CA 92161, USA
    J Immunol 180:7565-73. 2008

Collaborators

Detail Information

Publications17

  1. ncbi The molecular pathology of rosacea
    Kenshi Yamasaki
    Division of Dermatology, University of California, San Diego, CA 92161, USA
    J Dermatol Sci 55:77-81. 2009
    ..This article discusses the possible molecular mechanisms for the pathogenesis of rosacea from current clinical observations and laboratory research...
  2. ncbi Staphylococcus epidermidis antimicrobial delta-toxin (phenol-soluble modulin-gamma) cooperates with host antimicrobial peptides to kill group A Streptococcus
    Anna L Cogen
    Division of Dermatology, University of California San Diego, San Diego, California, United States of America
    PLoS ONE 5:e8557. 2010
    ..Thus, these data suggest that S. epidermidis-derived delta-toxin cooperates with the host-derived antimicrobial peptides in the innate immune system to reduce survival of an important human bacterial pathogen...
  3. ncbi Increased serine protease activity and cathelicidin promotes skin inflammation in rosacea
    Kenshi Yamasaki
    Division of Dermatology, University of California, San Diego, and VA San Diego Health Care System, 3350 La Jolla Village Drive, San Diego, California 92161, USA
    Nat Med 13:975-80. 2007
    ..These findings confirm the role of cathelicidin in skin inflammatory responses and suggest an explanation for the pathogenesis of rosacea by demonstrating that an exacerbated innate immune response can reproduce elements of this disease...
  4. ncbi TLR2 expression is increased in rosacea and stimulates enhanced serine protease production by keratinocytes
    Kenshi Yamasaki
    Division of Dermatology, Department of Medicine, University of California, San Diego, VA San Diego Health Care System, San Diego, California, USA
    J Invest Dermatol 131:688-97. 2011
    ..These observations show that abnormal TLR2 function may explain enhanced inflammatory responses to environmental stimuli and can act as a critical element in the pathogenesis of rosacea...
  5. ncbi Cathelicidin antimicrobial peptides inhibit hyaluronan-induced cytokine release and modulate chronic allergic dermatitis
    Yasuhide Morioka
    Division of Dermatology, University of California, San Diego, and Veterans Affairs San Diego Health Care System, San Diego, California 92161, USA
    J Immunol 181:3915-22. 2008
    ..These results suggest that cathelicidin has anti-inflammatory activity in skin that may be mediated in part by inhibition of HA-mediated processes...
  6. ncbi NLRP3/cryopyrin is necessary for interleukin-1beta (IL-1beta) release in response to hyaluronan, an endogenous trigger of inflammation in response to injury
    Kenshi Yamasaki
    Division of Dermatology, University of California, and Veterans Affairs San Diego Health Care System, San Diego, CA 92161, USA
    J Biol Chem 284:12762-71. 2009
    ..These findings support the hypothesis that hyaluronan works through IL-1beta and the cryopyrin system to signal sterile inflammation...
  7. ncbi Engagement of CD44 by hyaluronan suppresses TLR4 signaling and the septic response to LPS
    Jun Muto
    Division of Dermatology, University of California, San Diego and VA San Diego Health Care System, San Diego, CA 92161, USA
    Mol Immunol 47:449-56. 2009
    ..Therefore, our results show that hyaluronan acts through TLR4, CD44 and A20 to stimulate a unique cellular response that can protect against the septic response to LPS...
  8. ncbi Cathelicidin antimicrobial peptide LL-37 in psoriasis enables keratinocyte reactivity against TLR9 ligands
    Shin Morizane
    Division of Dermatology, Department of Medicine, University of California, San Diego and VA San Diego Healthcare System, San Diego, California, USA
    J Invest Dermatol 132:135-43. 2012
    ..These findings suggest that keratinocytes recognize and respond to DNA and can actively participate in contributing to the immunological environment that characterizes psoriasis...
  9. ncbi Selective antimicrobial action is provided by phenol-soluble modulins derived from Staphylococcus epidermidis, a normal resident of the skin
    Anna L Cogen
    Division of Dermatology, Department of Medicine, University of California San Diego, VA San Diego Health Care System, San Diego, California, USA
    J Invest Dermatol 130:192-200. 2010
    ..Thus, these data suggest that the production of PSMgamma and PSMdelta by S. epidermidis can benefit cutaneous immune defense by selectively inhibiting the survival of skin pathogens while maintaining the normal skin microbiome...
  10. ncbi Mast cell cathelicidin antimicrobial peptide prevents invasive group A Streptococcus infection of the skin
    Anna Di Nardo
    Department of Medicine, Division of Dermatology, University of California, San Diego and Veteran s Affairs Medical Center San Diego, CA 92161, USA
    J Immunol 180:7565-73. 2008
    ..Combined, these results show that MC confer defense against Gram-positive bacterial infection in the skin, a function mediated in part by the expression of a unique cathelicidin peptide...
  11. ncbi Kallikrein expression and cathelicidin processing are independently controlled in keratinocytes by calcium, vitamin D(3), and retinoic acid
    Shin Morizane
    Division of Dermatology, Department of Medicine, University of California, San Diego, San Diego, CA, USA
    J Invest Dermatol 130:1297-306. 2010
    ..Thus, these variables may further control the functions of antimicrobial peptides in the skin...
  12. ncbi Kallikrein-mediated proteolysis regulates the antimicrobial effects of cathelicidins in skin
    Kenshi Yamasaki
    Division of Dermatology, University of California, San Diego, and VA San Diego Health Care System, San Diego, California, USA
    FASEB J 20:2068-80. 2006
    ..These observations demonstrate that the balance of proteolytic activity at an epithelial interface will control innate immune defense...
  13. ncbi CC chemokine ligand 3 overcomes the bacteriocidal and phagocytic defect of macrophages and hastens recovery from experimental otitis media in TNF-/- mice
    Anke Leichtle
    Division of Otolaryngology, Department of Surgery, University of California, San Diego, La Jolla, CA 92093, USA
    J Immunol 184:3087-97. 2010
    ..Manipulation of CCL3 and/or TNF may prove to be effective therapeutic approaches in OM or other conditions associated with defective TNF generation...
  14. ncbi Exogenous addition of a C-xylopyranoside derivative stimulates keratinocyte dermatan sulfate synthesis and promotes migration
    Jun Muto
    Division of Dermatology, University of California, San Diego and Veterans Affairs San Diego Health Care System, San Diego, California, United States of America
    PLoS ONE 6:e25480. 2011
    ..These results indicate that C-Xyloside may enhance epithelial repair by serving as an initiator of DS synthesis...
  15. ncbi Antimicrobial peptides in human skin disease
    Kenshi Yamasaki
    Division of Dermatology, University of California, San Diego MC 9111B, San Diego, California 92161, USA
    Eur J Dermatol 18:11-21. 2008
    ....
  16. ncbi Recognition of hyaluronan released in sterile injury involves a unique receptor complex dependent on Toll-like receptor 4, CD44, and MD-2
    Kristen R Taylor
    Division of Dermatology, University of California, San Diego and Veterans Affairs Medical Center, San Diego, California 92161, USA
    J Biol Chem 282:18265-75. 2007
    ..Taken together, our results define a previously unknown mechanism for initiation of sterile inflammation that involves recognition of released hyaluronan fragments as an endogenous signal of tissue injury...
  17. ncbi Control of the innate epithelial antimicrobial response is cell-type specific and dependent on relevant microenvironmental stimuli
    Jürgen Schauber
    Division of Dermatology, University of California, San Diego and VA San Diego Healthcare System, San Diego, CA, USA
    Immunology 118:509-19. 2006
    ....